Regulation of systemic blood pressure. But what about the situation from a physiological point of view? Methods and instruments for measuring blood pressure

Blood pressure. Physiology.

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Blood pressure- blood pressure on the walls of blood vessels and chambers of the heart; the most important energy parameter of the circulatory system, ensuring continuity of blood flow in blood vessels, diffusion of gases and filtration of solutions of blood plasma ingredients through capillary membranes in tissue (metabolism), as well as in the renal glomeruli (urine formation).

In accordance with the anatomical-physiological division of cardio-vascular system a distinction is made between intracardiac, arterial, capillary and venous blood pressure, measured either in millimeters of water (in the veins) or millimeters of mercury (in other vessels and in the heart). Recommended, according to the International System of Units (SI), the expression of values ​​of efficiency in pascals (1 mmHg st. = 133,3 Pa) V medical practice not used. In arterial vessels, where K. d., as in the heart, varies significantly depending on the phase cardiac cycle, distinguish between systolic and diastolic (at the end of diastole) blood pressure, as well as pulse amplitude of fluctuations (the difference between the values ​​​​of systolic and diastolic blood pressure), or pulse blood pressure. The average value of the changes over the entire cardiac cycle, which determines average speed blood flow in the vessels is called mean hemodynamic pressure.

Measurement K. d. refers to the most widely used additional methods examination of the patient , since, firstly, the detection of changes in K. is important in the diagnosis of many diseases of the cardiovascular system and various pathological conditions; secondly, a pronounced increase or decrease in K. in itself can be the cause of severe hemodynamic disorders that threaten the patient's life. The most common measurement of blood pressure in the systemic circulation. In a hospital, if necessary, measure the pressure in the cubital or other peripheral veins; V specialized departments With diagnostic purpose K. is often measured in the cavities of the heart, the aorta, in the pulmonary trunk, and sometimes in the vessels of the portal system. To assess some important parameters of systemic hemodynamics, in some cases it is necessary to measure central venous pressure - the pressure in the superior and inferior vena cava.

PHYSIOLOGY

Blood pressure is characterized by the force with which blood acts on the walls of blood vessels perpendicular to their surface. The value of K. d. in each this moment reflects the level of potential mechanical energy in the vascular bed, which, with a pressure drop, can be transformed into the kinetic energy of blood flow in the vessels or into the work spent on filtering solutions through capillary membranes. As energy is spent to support these processes, efficiency decreases.

One of the most important conditions for the formation of blood vessels in blood vessels is their filling with blood in a volume commensurate with the capacity of the vascular cavity. The elastic walls of blood vessels provide elastic resistance to their stretching by the volume of pumped blood, which normally depends on the degree of smooth muscle tension, i.e. vascular tone. In an isolated vascular chamber, the elastic tension forces of its walls generate forces in the blood that balance them - pressure. The higher the tone of the chamber walls, the smaller its capacity and the higher the blood pressure, with a constant volume of blood contained in the chamber, and with a constant vascular tone, the higher the blood volume pumped into the chamber, the higher the blood pressure. Under real circulatory conditions, the dependence of blood pressure on the volume of blood contained in the vessels (the volume of circulating blood) is less clear than in the conditions of an isolated vessel, but it manifests itself in the case of pathological changes in the mass of circulating blood, for example, a sharp drop in blood pressure during massive blood loss or a decrease in plasma volume due to dehydration. K. d. drops similarly. at pathological increase capacity of the vascular bed, for example due to acute systemic venous hypotension.

The main energy source for pumping blood and creating blood pressure in the cardiovascular system is the work of the heart as a pressure pump. An auxiliary role in the formation of blood pressure is played by external compression of blood vessels (mainly capillaries and veins) by contracting skeletal muscles, periodic wave-like contractions of the veins, as well as the effect of gravity (blood weight), which especially affects the value of blood pressure in the veins.

^ Intracardiac pressure in the cavities of the atria and ventricles of the heart varies significantly in the phases of systole and diastole, and in the thin-walled atria it also significantly depends on fluctuations in intrathoracic pressure during the phases of breathing, sometimes taking negative values ​​in the inhalation phase. At the beginning of diastole, when the myocardium is relaxed, the chambers of the heart are filled with blood at a minimum pressure in them, close to zero. During atrial systole, there is a slight increase in pressure in them and in the ventricles of the heart. Pressure in the right atrium, normally not exceeding 2-3 mmHg st., is taken as the so-called phlebostatic level, in relation to which the value of Kd in the veins and other vessels of the systemic circulation is assessed.

During ventricular systole, when the heart valves are closed, almost all the contraction energy of the ventricular muscles is spent on volumetric compression of the blood contained in them, generating reactive tension in it in the form of pressure. Intraventricular pressure increases until in the left ventricle it exceeds the pressure in the aorta, and in the right - the pressure in the pulmonary trunk, due to which the valves of these vessels open and blood is expelled from the ventricles, at the end of which diastole begins, and K D. in the ventricles drops sharply.

^ Arterial pressure is formed due to the energy of the systole of the ventricles during the period of expulsion of blood from them, when each ventricle and the arteries of the corresponding circle of blood circulation become a single chamber, and the compression of the blood by the walls of the ventricles extends to the blood in the arterial trunks, and the portion of blood expelled into the arteries acquires a kinetic energy equal to half product of the mass of this portion by the square of the expulsion rate. Accordingly, the energy imparted to the arterial blood during the expulsion period has the same large values, the larger the stroke volume of the heart and the higher the ejection rate, depending on the magnitude and rate of increase of intraventricular pressure, i.e. on the power of ventricular contraction. The jerky, shock-like flow of blood from the ventricles of the heart causes local stretching of the walls of the aorta and pulmonary trunk and generates a pressure shock wave, the propagation of which, with the movement of local stretching of the wall along the length of the artery, causes the formation of arterial pulse ; the graphic display of the latter in the form of a sphygmogram or plethysmogram also corresponds to the display of the dynamics of blood pressure in the vessel according to the phases of the cardiac cycle.

The main reason for the transformation of most of the energy of cardiac output into arterial pressure, and not into the kinetic energy of the flow, is the resistance to blood flow in the vessels (the greater, the smaller their lumen, the greater their length and the higher the viscosity of the blood), formed mainly on the periphery of the arterial bed, in small arteries and arterioles, called resistance vessels, or resistive vessels. Obstruction of blood flow at the level of these vessels creates flow inhibition in the arteries proximal to them and conditions for blood compression during the period of expulsion of its systolic volume from the ventricles. The higher the peripheral resistance, the larger part of the cardiac output energy is transformed into a systolic increase in blood pressure, determining the value of pulse pressure (partially the energy is transformed into heat from the friction of blood against the walls of blood vessels). The role of peripheral resistance to blood flow in the formation of blood pressure is clearly illustrated by the differences in blood pressure in the systemic and pulmonary circulation. In the latter, which has a shorter and wider vascular bed, the resistance to blood flow is much less than in the systemic circulation, therefore, at equal rates of expulsion of the same systolic volumes of blood from the left and right ventricles, the pressure in the pulmonary trunk is approximately 6 times less than in the aorta.

Systolic blood pressure is the sum of pulse and diastolic pressure. Its true value, called lateral systolic blood pressure, can be measured using a manometric tube inserted into the lumen of the artery perpendicular to the axis of blood flow. If you suddenly stop the blood flow in the artery by completely clamping it distal to the manometric tube (or positioning the lumen of the tube against the blood flow), then systolic blood pressure immediately increases due to the kinetic energy of the blood flow. This higher value of blood pressure is called final, or maximum, or full, systolic blood pressure, because it is equivalent to almost the total energy of the blood during systole. Both lateral and maximum systolic blood pressure in the arteries of human limbs can be measured bloodlessly using arterial tachooscillography according to Savitsky. When measuring blood pressure according to Korotkoff, the values ​​of maximum systolic blood pressure are determined. Its normal value at rest is 100-140 mmHg st., lateral systolic blood pressure is usually 5-15 mm below the maximum. The true value of pulse blood pressure is determined as the difference between the lateral systolic and diastolic pressure.

Diastolic blood pressure is formed due to the elasticity of the walls of the arterial trunks and their large branches, which together form extensible arterial chambers, called compression chambers (aortoarterial chamber in the systemic circulation and the pulmonary trunk with its large branches in the pulmonary circulation). In a system of rigid tubes, stopping the pumping of blood into them, as happens in diastole after the closure of the aortic and pulmonary valves, would lead to a rapid disappearance of the pressure that appeared during systole. In a real vascular system, the energy of the systolic increase in blood pressure is largely accumulated in the form of elastic stress of the stretched elastic walls of the arterial chambers. The higher the peripheral resistance to blood flow, the longer these elastic forces provide volumetric compression of the blood in the arterial chambers, maintaining K. d., the value of which, as the blood outflows into the capillaries and the walls of the aorta and pulmonary trunk collapse, gradually decreases towards the end of diastole (the greater the longer than diastole). Normally, diastolic blood pressure in the arteries of the systemic circulation is 60-90 mmHg st. With normal or increased cardiac output (minute volume of blood circulation), an increase in heart rate (short diastole) or a significant increase in peripheral resistance to blood flow causes an increase in diastolic blood pressure, since equality of blood outflow from the arteries and blood flow into them from the heart is achieved with greater stretching and, therefore, greater elastic stress on the walls of the arterial chambers at the end of diastole. If the elasticity of arterial trunks and large arteries is lost (for example, when atherosclerosis ), then diastolic blood pressure decreases, because part of the cardiac output energy, normally accumulated by the stretched walls of the arterial chambers, is spent on an additional increase in systolic blood pressure (with an increase in pulse rate) and acceleration of blood flow in the arteries during the ejection period.

The average hemodynamic, or average, K. d. is average value from all its variable values ​​for the cardiac cycle, defined as the ratio of the area under the curve of pressure changes to the duration of the cycle. In the arteries of the extremities, the average blood pressure can be determined quite accurately using tachooscillography. Normally, it is 85-100 mmHg st., approaching the value of diastolic blood pressure, the greater the longer the diastole. Average blood pressure does not have pulse fluctuations and can change only in the interval of several cardiac cycles, being therefore the most stable indicator of blood energy, the values ​​of which are determined almost only by the values ​​of the minute volume of blood supply and the total peripheral resistance to blood flow.

In arterioles that offer the greatest resistance to blood flow, a significant portion of the total energy of arterial blood is spent to overcome it; pulse fluctuations K. d. in them are smoothed out, the average K. d. in comparison with the intra-aortic one is reduced by approximately 2 times.

^ Capillary pressure depends on the pressure in the arterioles. The walls of the capillaries do not have tone; the total lumen of the capillary bed is determined by the number of open capillaries, which depends on the function of the precapillary sphincters and the value of K. d. in the precapillaries. Capillaries open and remain open only with positive transmural pressure - the difference between the pressure inside the capillary and the tissue pressure compressing the capillary from the outside. The dependence of the number of open capillaries on the KD in the precapillaries provides a kind of self-regulation of the constancy of the capillary KD. The higher the KD in the precapillaries, the more numerous the open capillaries, the greater their lumen and capacity, and therefore the more the KD drops. d. on the arterial segment of the capillary bed. Thanks to this mechanism, the average efficiency in capillaries is relatively stable; on the arterial segments of the capillaries of the systemic circulation it is 30-50 mmHg st., and on the venous segments, due to the energy consumption to overcome resistance along the length of the capillary and filtration, it decreases to 25-15 mmHg st. The magnitude of venous pressure has a significant influence on capillary blood pressure and its dynamics along the capillary.

^ Venous pressure in the postcapillary segment differs little from the pressure in the venous part of the capillaries, but drops significantly along the venous bed, reaching a value in the central veins close to the pressure in the atrium. In peripheral veins located at the level of the right atrium. K. d. normally rarely exceeds 120 mm water st., which is commensurate with the pressure of the blood column in the veins lower limbs with a vertical body position. The participation of the gravitational factor in the formation of venous pressure is least when the body is in a horizontal position. Under these conditions, blood pressure in the peripheral veins is formed mainly due to the energy of the influx of blood into them from the capillaries and depends on the resistance to the outflow of blood from the veins (normally, mainly from intrathoracic and intraatrial pressure) and, to a lesser extent, on the tone of the veins, which determines their capacity for blood at a given pressure and, accordingly, the rate of venous return of blood to the heart. The pathological growth of venous K. d. in most cases is due to a violation of the outflow of blood from them.

The relatively thin wall and large surface of the veins create the prerequisites for a pronounced influence on venous blood pressure changes in external pressure associated with contraction of skeletal muscles, as well as atmospheric (in the skin veins), intrathoracic (especially in the central veins) and intra-abdominal (in the system portal vein) pressure. In all veins, blood pressure fluctuates depending on the phases of the respiratory cycle, decreasing in most of them during inhalation and increasing during exhalation. In patients with bronchial obstruction, these fluctuations are detected visually when examining the neck veins, which swell sharply during the exhalation phase and completely collapse during inspiration. Pulse oscillations of blood pressure in most parts of the venous bed are weakly expressed, being mainly transmitted from the pulsation of arteries located next to the veins (pulse oscillations of blood pressure in the right atrium can be transmitted to the central and close veins, which is reflected in the venous pulse ). An exception is the portal vein, in which the blood pressure may have pulse fluctuations, which are explained by the appearance during cardiac systole of the so-called hydraulic valve for the passage of blood through it to the liver (due to the systolic increase in blood pressure in the hepatic artery basin) and subsequent (during cardiac diastole) by expulsion of blood from the portal vein to the liver.

^ Meaning blood pressure for the functioning of the body is determined by the special role of mechanical energy for the functions of blood as a universal mediator in the metabolism and energy in the body, as well as between the body and the environment. Discrete portions of mechanical energy generated by the heart only during systole are converted in blood pressure into a stable source of energy supply for the transport function of the blood, gas diffusion and filtration processes in the capillary bed, which is active during the diastole of the heart, ensuring the continuity of metabolism and energy in the body. and mutual regulation of the functions of various organs and systems by humoral factors carried in the circulating blood.

Kinetic energy is only a small part of the total energy imparted to the blood by the work of the heart. The main energy source of blood movement is the pressure difference between the initial and final segments of the vascular bed. In the systemic circulation, such a drop, or total gradient, of pressure corresponds to the difference in the values ​​of the average blood pressure in the aorta and in the vena cava, which is normally almost equal to the value of the average blood pressure. The average volumetric velocity of blood flow, expressed, for example, by the minute volume of blood circulation, is directly proportional to the total pressure gradient, i.e. practically the value of average blood pressure, and is inversely proportional to the value of total peripheral resistance to blood flow. This dependence underlies the calculation of the value of total peripheral resistance as the ratio of mean blood pressure to minute volume of blood circulation. In other words, the higher the average blood pressure at a constant resistance, the higher the blood flow in the vessels and the greater the mass of substances exchanged in tissues (mass transfer) is transported per unit time by blood through the capillary bed. However, under physiological conditions, an increase in minute volume of blood circulation, necessary to intensify tissue respiration and metabolism, for example when physical activity, as well as its rational reduction for resting conditions, is achieved mainly by the dynamics of peripheral resistance to blood flow, and in such a way that the value of average blood pressure is not subject to significant fluctuations. Relative stabilization of mean blood pressure in the aortoarterial chamber with the help of special mechanisms of its regulation creates the possibility of dynamic variations in the distribution of blood flow between organs according to their needs through only local changes in blood flow resistance.

An increase or decrease in the mass exchange of substances on capillary membranes is achieved by changes in the volume of capillary blood flow and membrane area that depend on the pressure, mainly due to changes in the number of open capillaries. At the same time, thanks to the mechanism of self-regulation of capillary blood pressure in each individual capillary, it is maintained at the level necessary for optimal mode mass transfer along the entire length of the capillary, taking into account the importance of ensuring a strictly defined degree of reduction in K. d. in the direction of the venous segment.

In each part of the capillary, mass transfer on the membrane directly depends on the value of efficiency in this particular part. For the diffusion of gases, for example oxygen, the value of efficiency is determined by the fact that diffusion occurs due to the difference in the partial pressure (voltage) of a given gas on both sides of the membrane, and this is part of the total pressure in the system (in the blood - part of the efficiency) , proportional to the volumetric concentration of a given gas. Filtration of solutions various substances through the membrane is provided by filtration pressure - the difference between the transmural pressure in the capillary and the oncotic pressure of the blood plasma, which is about 30 on the arterial segment of the capillary mmHg st. Since in this segment the transmural pressure is higher than the oncotic pressure, aqueous solutions of substances are filtered through the membrane from the plasma into the intercellular space. Due to water filtration, the concentration of proteins in the capillary blood plasma increases, and oncotic pressure increases, reaching transmural pressure in the middle part of the capillary (filtration pressure decreases to zero). On the venous segment, due to a drop in pressure along the length of the capillary, the transmural pressure becomes lower than the oncotic pressure (filtration pressure becomes negative), so aqueous solutions are filtered from the intercellular space into the plasma, reducing its oncotic pressure to the original values. Thus, the degree of drop in blood pressure along the length of the capillary determines the ratio of the areas of filtration of solutions through the membrane from the plasma into the intercellular space and back, thereby affecting the balance of water exchange between blood and tissues. In the case of a pathological increase in venous blood pressure, the filtration of fluid from the blood in the arterial part of the capillary exceeds the return of fluid to the blood in the venous segment, which leads to fluid retention in the intercellular space, the development edema .

Features of the structure of glomerular capillaries kidney provide a high level of K. d. and positive filtration pressure throughout the capillary loops of the glomerulus, which contributes to a high rate of formation of extracapillary ultrafiltrate - primary urine. The pronounced dependence of the urinary function of the kidneys on blood pressure in the arterioles and capillaries of the glomeruli explains the special physiological role renal factors in the regulation of blood pressure in the arteries are more important in the circulation.

^ Mechanisms of blood pressure regulation . K. stability in the body is ensured functional systems , maintaining an optimal level of blood pressure for tissue metabolism. The main principle in the activity of functional systems is the principle of self-regulation, thanks to which healthy body any episodic fluctuations in blood pressure caused by physical or emotional factors stop after a certain time, and blood pressure returns to its original level. The mechanisms of self-regulation of blood pressure in the body suggest the possibility of dynamic formation of opposite ultimate impact on K. d. changes in hemodynamics, called pressor and depressor reactions, as well as the presence of a system feedback. Pressor reactions leading to an increase in blood pressure are characterized by an increase in minute volume of blood circulation (due to an increase in systolic volume or increased heart rate with a constant systolic volume), an increase in peripheral resistance as a result of vasoconstriction and an increase in blood viscosity, an increase in circulating blood volume, etc. Depressor reactions , aimed at lowering blood pressure, are characterized by a decrease in minute and systolic volumes, a decrease in peripheral hemodynamic resistance due to dilation of arterioles and a decrease in blood viscosity. A unique form of blood pressure regulation is the redistribution of regional blood flow, in which an increase in blood pressure and blood volume velocity in vital organs (heart, brain) is achieved through a short-term decrease in these indicators in other organs that are less significant for the existence of the body.

K. regulation is carried out by a complex of complex interacting nervous and humoral influences on vascular tone and heart activity. The control of pressor and depressor reactions is associated with the activity of the bulbar vasomotor centers, controlled by the hypothalamic, limbic-reticular structures and cerebral cortex, and is realized through changes in the activity of parasympathetic and sympathetic nerves regulating vascular tone, the activity of the heart, kidneys and endocrine glands, the hormones of which are involved in the regulation of blood pressure. Among the latter highest value have ACTH and vasopressin of the pituitary gland, adrenaline and hormones of the adrenal cortex, as well as hormones of the thyroid and gonads. The humoral link in the regulation of blood pressure is also represented by the renin-angiotensin system, the activity of which depends on the blood supply and kidney function, prostaglandins and a number of other vasoactive substances of various origins (aldosterone, kinins, vasoactive intestinal peptide, histamine, serotonin, etc.). Rapid regulation of blood pressure, necessary, for example, when changes in body position, level of physical or emotional stress, is carried out mainly by the dynamics of the activity of the sympathetic nerves and the flow of adrenaline into the blood from the adrenal glands. Adrenaline and norepinephrine, released at the ends of the sympathetic nerves, excite the -adrenergic receptors of blood vessels, increasing the tone of the arteries and veins, and the -adrenergic receptors of the heart, increasing cardiac output, i.e. determine the development of the pressor reaction.

The feedback mechanism that determines changes in the degree of activity of the vasomotor centers opposite to deviations in the value of Kd. in the vessels is provided by the function of baroreceptors in the cardiovascular system, of which the baroreceptors of the sinocarotid zone and renal arteries are of greatest importance. With an increase in blood pressure, the baroreceptors of the reflexogenic zones are excited, the depressor effects on the vasomotor centers are enhanced, which leads to a decrease in sympathetic and an increase in parasympathetic activity with a simultaneous decrease in the formation and release of hypertensive substances. As a result, the pumping function of the heart decreases, peripheral vessels dilate and, as a result, blood pressure decreases. When blood pressure decreases, opposite effects appear: sympathetic activity increases, pituitary-adrenal mechanisms and the renin-angiotensin system are activated.

The secretion of renin by the juxtaglomerular apparatus of the kidneys naturally increases with a decrease in pulse blood pressure in the renal arteries, with renal ischemia, and also with sodium deficiency in the body. Renin converts one of the blood proteins (angiotensinogen) into angiotensin I, which is a substrate for the formation of angiotensin II in the blood, which, when interacting with specific vascular receptors, causes a powerful pressor reaction. One of the angiotensin conversion products (angiotensin III) stimulates the secretion of aldosterone, which changes water-salt metabolism, which also affects the value of Kd. The process of formation of angiotensin II occurs with the participation of angiotensin-converting enzymes, the blockade of which, like the blockade of angiotensin II receptors in blood vessels, eliminates the hypertensive effects associated with the activation of the renin-angiotensin system.

^ BLOOD PRESSURE IS NORMAL

The value of K. in healthy individuals has significant individual differences and is subject to noticeable fluctuations under the influence of changes in body position, environmental temperature, emotional and physical stress, and for arterial K. its dependence is also noted on gender, age, lifestyle, body weight, degree of physical fitness.

Blood pressure in the pulmonary circulation is measured during special diagnostic studies directly by probing the heart and pulmonary trunk. In the right ventricle of the heart, both in children and adults, the value of systolic K. d. normally varies from 20 to 30, and diastolic - from 1 to 3 mmHg st., more often determined in adults at the level of average values ​​of 25 and 2, respectively mmHg st.

In the pulmonary trunk under resting conditions, the range of normal values ​​of systolic blood pressure is in the range of 15-25, diastolic - 5-10, average - 12-18 mmHg st.; in children preschool age diastolic blood pressure is usually 7-9, average - 12-13 mmHg st. When straining, K. d. in the pulmonary trunk can increase several times.

Blood pressure in the pulmonary capillaries is considered normal when its values ​​at rest are from 6 to 9 mmHg st. sometimes it reaches 12 mmHg st.; usually its value in children is 6-7, in adults - 7-10 mmHg st.

In the pulmonary veins, the average K. d. ranges from 4 to 8 mmHg st., i.e. exceeds the average K. d. in the left atrium, which is 3-5 mmHg st. According to the phases of the cardiac cycle, pressure in the left atrium ranges from 0 to 9 mmHg st.

Blood pressure in the systemic circulation is characterized by the greatest difference - from the maximum value in the left ventricle and aorta to the minimum in the right atrium, where at rest it usually does not exceed 2-3 mmHg st., often taking negative values ​​in the inhalation phase. In the left ventricle of the heart, K. d. at the end of diastole is 4-5 mmHg st., and during the period of systole increases to a value commensurate with the value of systolic K. d. in the aorta. The limits of normal values ​​​​of systolic K. d. in the left ventricle of the heart are 70-110 in children, and 100-150 in adults mmHg st.

^ Arterial pressure when measured on the upper limbs according to Korotkov in adults at rest, it is considered normal in the range from 100/60 to 150/90 mmHg st. However, in fact, the range of normal individual BP values ​​is wider, and BP is about 90/50. mmHg st. often determined in perfectly healthy individuals, especially those engaged in physical labor or sports. On the other hand, the dynamics of blood pressure in the same person within the range of values ​​considered normal may actually reflect pathological changes in blood pressure. The latter must be borne in mind, first of all, in cases where such dynamics is exceptional against the background of relatively stable blood pressure values ​​in a given person (for example, a decrease in blood pressure to 100/60 from the usual values ​​for a given individual of about 140/90 mmHg st. or vice versa).

It was noted that in the normal range, blood pressure in men is higher than in women; higher values ​​of blood pressure are recorded in obese subjects, urban residents, people of mental labor, lower ones - in rural residents, who are constantly engaged in physical labor, sports. In the same person, blood pressure can clearly change under the influence of emotions, with a change in body position, in accordance with daily rhythms (in most healthy people, blood pressure rises in the afternoon and evening and decreases after 2 h nights). All these fluctuations occur mainly due to changes in systolic blood pressure with a relatively stable diastolic.

To assess blood pressure as normal or pathological, it is important to take into account the dependence of its magnitude on age, although this dependence, which is clearly expressed statistically, is not always manifested in individual blood pressure values.

Children under 8 years of age have lower blood pressure than adults. In newborns, systolic blood pressure is close to 70 mmHg st., in the coming weeks of life, it rises and by the end of the first year of a child's life reaches 80-90 with a diastolic blood pressure value of about 40 mmHg st. In subsequent years of life, blood pressure gradually increases, and at 12-14 years of age in girls and 14-16 years of age in boys, an accelerated increase in blood pressure values ​​is observed to values ​​comparable to blood pressure in adults. In children aged 7 years, blood pressure ranges from 80-110/40-70, in children aged 8-13 years - 90-120/50-80 mmHg st., and in girls 12 years old it is higher than in boys of the same age, and in the period between 14 and 17 years old blood pressure reaches values ​​of 90-130/60-80 mmHg st., and on average it becomes higher for boys than for girls. As in adults, differences in blood pressure were noted in children living in the city and in rural areas, as well as its fluctuations during various loads. Blood pressure is noticeable (up to 20 mmHg st.) increases when the child is excited, when sucking (in infants), when the body is cooled; When overheated, for example in hot weather, blood pressure decreases. In healthy children, after the end of the cause of the increase in blood pressure (for example, the act of sucking), it occurs quickly (within approximately 3-5 min) decreases to the original level.

The increase in blood pressure with age in adults occurs gradually, somewhat accelerating in old age. Systolic blood pressure increases mainly due to a decrease in the elasticity of the aorta and large arteries in old age, however, even in old healthy people, resting blood pressure does not exceed 150/90 mmHg st. At physical work or emotional stress blood pressure may increase to 160/95 mmHg st., and the restoration of its initial level at the end of the load occurs more slowly than in young people, which is associated with age-related changes blood pressure regulation apparatus - a decrease in the regulatory function of the neuro-reflex link and an increase in the role of humoral factors in the regulation of blood pressure. For an approximate assessment of normal blood pressure in adults, depending on gender and age, various formulas have been proposed, for example, a formula for calculating the normal value of systolic blood pressure as the sum of two numbers, one of which is equal to the age of the subject in years, the other is 65 for men and 55 for women. However, the high individual variability of normal blood pressure values ​​makes it preferable to focus on the degree of increase in blood pressure over the years in a particular person and assess the pattern of blood pressure values ​​approaching upper limit normal values, i.e. to 150/90 mmHg st. when measured at rest.

^ Capillary pressure in the systemic circulation varies somewhat in the basins of different arteries. In most capillaries, on their arterial segments, ko fluctuates between 30-50, on venous segments - 15-25 mmHg st. In the capillaries of the mesenteric arteries, K. d., according to some studies, can be 10-15, and in the network of portal vein ramifications - 6-12 mmHg st. Depending on changes in blood flow in accordance with the needs of the organs, the value of K. d. in their capillaries may change.

^ Venous pressure largely depends on the place of its measurement, as well as on the position of the body. Therefore, for comparison of indicators, venous K. is measured in a horizontal position of the body. Along the venous bed, K. d. decreases; in venules it is 150-250 mm water st., in the central veins ranges from + 4 to - 10 mm water st. In the cubital vein in healthy adults, the Kd value is usually determined between 60 and 120 mm water st.; K.d. values ​​in the range of 40-130 are considered normal mm water st., but deviations in the Kd value beyond 30-200 really have clinical significance mm water st.

The dependence of venous blood pressure on the age of the subjects is revealed only statistically. In children it increases with age - on average from 40 to 100 mm water st.; in older people there is a tendency to decrease venous blood pressure, which is associated with an increase in the capacity of the venous bed due to an age-related decrease in the tone of the veins and skeletal muscles.

^ PATHOLOGICAL CHANGES IN BLOOD PRESSURE

Deviations of blood pressure from normal values ​​have important clinical significance as symptoms of pathology of the circulatory system or its regulatory systems. Pronounced changes in blood pressure are themselves pathogenic, causing disturbances in general blood circulation and regional blood flow and playing a leading role in the formation of such dangerous pathological conditions as collapse , shock , hypertensive crises , pulmonary edema .

Changes in blood pressure in the cavities of the heart are observed with myocardial lesions, significant deviations in blood pressure values ​​in the central arteries and veins, as well as with disturbances of intracardiac hemodynamics, and therefore measurement of intracardiac blood pressure is carried out for the diagnosis of congenital and acquired defects heart and large vessels. An increase in blood pressure in the right or left atria (with heart defects, heart failure) leads to a systemic increase in pressure in the veins of the systemic or pulmonary circulation.

^ Arterial hypertension , i.e. pathological increase Blood pressure in the main arteries of the systemic circulation (up to 160/100 mmHg st. and more), may be due to an increase in stroke and cardiac output, increased kinetics of cardiac contraction, and rigidity of the walls of the arterial compression chamber, but in most cases it is determined by a pathological increase in peripheral resistance to blood flow (see. Arterial hypertension ). Since the regulation of blood pressure is carried out by a complex set of neurohumoral influences with the participation of the central nervous system, renal, endocrine and other humoral factors, arterial hypertension can be a symptom of various diseases, incl. kidney diseases - glomerulonephritis (see. Jades ), pyelonephritis , urolithiasis , hormonally active pituitary tumors (see. Itsenko - Cushing's disease ) and adrenal glands (for example, aldosteromes, chromaffinoma . ), thyrotoxicosis ; organic diseases of the central nervous system; hypertension . Increased blood pressure in the pulmonary circulation (see. Hypertension of the pulmonary circulation ) may be a symptom of pathology of the lungs and pulmonary vessels (in particular, pulmonary embolism ), pleura, chest, hearts. Sustained arterial hypertension leads to cardiac hypertrophy, the development of myocardial dystrophy and may be the cause heart failure .

A pathological decrease in blood pressure may be a consequence of myocardial damage, incl. acute (for example, with myocardial infarction ), reducing peripheral resistance to blood flow, blood loss, sequestration of blood in capacitance vessels with insufficient venous tone. It shows up orthostatic circulatory disorders , and with an acute, pronounced drop in blood pressure - a picture of collapse, shock, anuria. Sustainable arterial hypotension observed in diseases accompanied by pituitary and adrenal insufficiency. When arterial trunks are occluded, blood pressure decreases only distal to the site of occlusion. A significant decrease in blood pressure in the central arteries due to hypovolemia includes adaptive mechanisms of the so-called centralization of blood circulation - redistribution of blood mainly into the vessels of the brain and heart during sharp increase vascular tone in the periphery. If these compensatory mechanisms are insufficient, fainting , ischemic brain damage (see. Stroke ) and myocardium (see. Cardiac ischemia ).

An increase in venous pressure is observed either in the presence of arteriovenous shunts, or in cases of disturbances in the outflow of blood from the veins, for example, as a result of their thrombosis, compression, or due to an increase in blood pressure in the atrium. In liver cirrhosis it develops portal hypertension .

Changes in capillary pressure are usually a consequence of primary changes in blood pressure in the arteries or veins and are accompanied by disturbances in blood flow in the capillaries, as well as in the processes of diffusion and filtration on capillary membranes (see. Microcirculation ). Hypertension in the venous part of the capillaries leads to the development of edema, general (with systemic venous hypertension) or local, for example with phlebothrombosis, compression of the veins (see. Stokes collar ). An increase in capillary blood pressure in the pulmonary circulation in the vast majority of cases is associated with a violation of the outflow of blood from the pulmonary veins to the left atrium. This occurs with left ventricular heart failure, mitral stenosis, the presence of a thrombus or tumor in the cavity of the left atrium, pronounced tachysystole with atrial fibrillation . Manifested by shortness of breath, cardiac asthma, and the development of pulmonary edema.

^ METHODS AND DEVICES FOR MEASURING BLOOD PRESSURE

In the practice of clinical and physiological research, methods for measuring arterial, venous and capillary pressure in the systemic circulation, in the central vessels of the pulmonary circulation, in individual organs and body parts. There are direct and indirect methods for measuring blood pressure. The latter are based on measuring external pressure on a vessel (for example, air pressure in a cuff placed on a limb), which balances blood pressure inside the vessel.

^ Direct blood pressure measurement (direct manometry) is carried out directly in the vessel or cavity of the heart, where the filled isotonic solution a catheter that transmits pressure to an external measuring device or probe with a transducer at the insertion end (see Catheterization ). In the 50-60s. 20th century direct manometry began to be combined with angiography, intracavitary phonocardiography, electrohisography, etc. Characteristic feature modern development direct manometry is computerization and automation of data processing. Direct measurement of blood pressure is carried out in almost any part of the cardiovascular system and serves as a basic method for checking the results of indirect blood pressure measurements. The advantage of direct methods is the possibility of simultaneous collection of blood samples through a catheter for biochemical tests and introduction of necessary medications and indicators into the bloodstream. The main disadvantage of direct measurements is the need to carry out elements of the measuring device into the bloodstream, which requires strict adherence to aseptic rules and limits the possibility of repeated measurements. Some types of measurements (catheterization of the cavities of the heart, pulmonary vessels, kidneys, brain) are actually surgical operations and are performed only in a hospital setting. Measurement of pressure in the cavities of the heart and central vessels possible only by the direct method. The measured quantities are instantaneous pressure in the cavities, average pressure and other indicators, which are determined by means of recording or indicating pressure gauges, in particular an electromanometer. The input link of the electromanometer is the sensor. Its sensitive element, the membrane, is in direct contact with the liquid medium through which pressure is transmitted. Movements of the membrane, typically fractions of a micron, are perceived as changes electrical resistance, capacitance or inductance, converted into electrical voltage measured by an output device. The method is a valuable source of physiological and clinical information and is used for diagnosis, in particular of heart defects, monitoring the effectiveness of surgical correction of central circulatory disorders, during long-term observations in intensive care conditions and in some other cases. Direct blood pressure measurement in humans it is carried out only in cases where constant and long-term monitoring of blood pressure levels is necessary in order to timely detect its dangerous changes. Such measurements are sometimes used in the practice of monitoring patients in intensive care units, as well as during some surgical operations. For capillary pressure measurements electromanometers are used; Stereoscopic and television microscopes are used to visualize vessels. A microcannula connected to a pressure gauge and a source of external pressure and filled with physiological solution is inserted into the capillary or its side branch using a micromanipulator under the control of a microscope. The average pressure is determined by the value of the external pressure created (set and recorded by a pressure gauge), at which the blood flow in the capillary stops. To study fluctuations in capillary pressure, continuous recording is used after insertion of a microcannula into the vessel. In diagnostic practice, measuring capillary blood pressure is practically not used. Venous pressure measurement also carried out by the direct method. A device for measuring venous blood pressure consists of an interconnected drip intravenous fluid infusion system, a manometric tube, and a rubber hose with an injection needle at the end. For one-time measurements of Kd., a drip infusion system is not used; it is connected when continuous long-term phlebotonometry is necessary, during which liquid is constantly supplied from the drip infusion system into the measuring line and from it into the vein. This eliminates thrombosis of the needle and makes it possible to measure venous pressure for many hours. The simplest venous pressure meters contain only a scale and a manometric tube made of plastic material, intended for single use. Electronic pressure gauges are also used to measure venous blood pressure (with their help, it is also possible to measure blood pressure in the right parts of the heart and pulmonary trunk). Central venous pressure is measured through a thin polyethylene catheter, which is inserted into the central veins through the ulnar saphenous or subclavian vein. During long-term measurements, the catheter remains attached and can be used to take blood samples and administer medications.

^ Indirect blood pressure measurement carried out without violating the integrity of blood vessels and tissues. Complete atraumaticity and the possibility of unlimited repeated measurements of pressure have led to the widespread use of these methods in practice diagnostic studies. Methods based on the principle of balancing the pressure inside a vessel with a known external pressure are called compression. Compression can be caused by liquid, air or a solid. The most common method of compression is using an inflatable cuff placed on a limb or vessel and providing uniform circular compression of tissues and vessels. The first compression cuff for measuring blood pressure was proposed in 1896 by S. Riva-Rocci. Changes in pressure external to the blood vessel during the measurement of blood pressure can have the character of a slow gradual increase in pressure (compression), a gradual decrease in the previously created high pressure (decompression), and also follow changes in intravascular pressure. The first two modes are used to determine discrete indicators of efficiency (maximum, minimum, etc.), the third - for continuous recording of efficiency, similar to the direct measurement method. As criteria for identifying the balance of external and intravascular pressures, sound, pulse phenomena, changes in blood supply to tissues and blood flow in them, as well as other phenomena caused by compression of blood vessels are used. Blood pressure measurement usually produced in the brachial artery, in which it is close to the aortic. In some cases, pressure is measured in the arteries of the thigh, leg, fingers and other areas of the body. Systolic blood pressure can be determined by manometer readings at the moment of vessel compression, when the pulsation of the artery in its distal part from the cuff disappears, which can be determined by palpation of the pulse on the radial artery (Riva-Rocci palpation method). The most common in medical practice is the sound, or auscultatory, method of indirect measurement of blood pressure according to Korotkov using a sphygmomanometer and phonendoscope (sphygmomanometry). In 1905 N.S. Korotkov found that if an external pressure exceeding the diastolic pressure is applied to the artery, sounds (tones, noises) arise in it, which stop as soon as the external pressure exceeds the systolic level. To measure blood pressure according to Korotkov, a special pneumatic cuff of the required size (depending on the age and physique of the subject) is tightly placed on the subject’s shoulder, which is connected through a tee to a pressure gauge and to a device for injecting air into the cuff. The latter usually consists of an elastic rubber bulb with check valve and a valve for slowly releasing air from the cuff (regulating the decompression mode). The design of the cuffs includes devices for fastening them, the most convenient of which are coating the fabric ends of the cuff with special materials that ensure adhesion of the connected ends and reliable retention of the cuff on the shoulder. Using a bulb, air is pumped into the cuff under the control of the pressure gauge readings to a pressure value that obviously exceeds systolic blood pressure, then, releasing the pressure from the cuff by slowly releasing air from it, i.e. in the mode of vessel decompression, simultaneously listen to the brachial artery in the ulnar bend using a phonendoscope and determine the moments of the appearance and cessation of sounds, comparing them with the readings of the pressure gauge. The first of these moments corresponds to systolic, the second - to diastolic pressure. Several types of sphygmomanometers are produced for measuring blood pressure using sound. The simplest are mercury and membrane manometers, on the scales of which blood pressure can be measured in the range of 0-260, respectively. mmHg st. and 20-300 mmHg st. with an error of ± 3 to ± 4 mmHg st. Less common are electronic blood pressure meters with sound and (or) light alarms and a dial or digital indicator of systolic and diastolic blood pressure. The cuffs of such devices have built-in microphones for the perception of Korotkoff tones. Various instrumental methods indirect blood pressure measurements based on recording changes in blood supply to the distal part of the limb during arterial compression (volumetric method) or the nature of oscillations associated with pressure pulsation in the cuff (arterial oscillography). A variation of the oscillatory method is arterial tachooscillography according to Savitsky, which is carried out using a mechanocardiograph (see. Mechanocardiography ). By characteristic changes Tachooscillograms during artery compression determine lateral systolic, mean and diastolic blood pressure. Other methods have been proposed for measuring mean blood pressure, but they are less common than tachooscillography. Capillary pressure measurement non-invasively was first carried out by N. Kries in 1875 by observing the change in skin color under the influence of externally applied pressure. The pressure at which the skin begins to turn pale is taken as the blood pressure in superficial capillaries. Modern indirect methods for measuring pressure in capillaries are also based on the compression principle. Compression is carried out by transparent small rigid chambers of various designs or transparent elastic cuffs, which are applied to the area under study (skin, nail bed, etc.). The compression site is well illuminated to observe the vasculature and blood flow in it under a microscope. Capillary pressure is measured during microvascular compression or decompression. In the first case, it is determined by the compression pressure at which blood flow will stop in most visible capillaries, in the second - by the level of compression pressure at which blood flow will occur in several capillaries. Indirect methods for measuring capillary pressure give significant discrepancies in results. Venous pressure measurement also possible indirect methods. For this, two groups of methods have been proposed: compression and so-called hydrostatic. Compression methods turned out to be unreliable and were not used. Of the hydrostatic methods, the simplest is the Gertner method. Observing the back of the hand as it is slowly raised, note the height at which the veins collapse. The distance from the level of the atrium to this point serves as an indicator of venous pressure. The reliability of this method is also low due to the lack of clear criteria for complete balancing of external and intravascular pressure. Nevertheless, its simplicity and accessibility make it useful for an approximate assessment of venous pressure during examination of a patient under any conditions.

Venous pressure(syn. venous blood pressure) - the pressure that the blood in the lumen of a vein exerts on its wall: the value of V.D. depends on the caliber of the vein, the tone of its walls, the volumetric velocity of blood flow and the value of intrathoracic pressure.

Maintaining a normal level of blood pressure in the main arteries is the most important condition necessary to ensure blood flow adequate to the needs of the body. Blood pressure level regulation is carried out by a complex multi-circuit functional system, which uses the principles of pressure regulation based on deviation and (or) disturbance. A diagram of such a system, built on the principles of the theory of functional systems by P.K. Anokhin, shown in Fig. 1.17. As in any other functional system for regulating the parameters of the internal environment of the body, it is possible to single out a regulated indicator, which is the level of blood pressure in the aorta, large arterial vessels and cavities of the heart.

Rice. 1.17.1-3 - impulses from extero-, intero-, proprioreceptors

Direct assessment of blood pressure levels is carried out by baroreceptors of the aorta, arteries and heart. These receptors are mechanoreceptors, formed by the endings of afferent nerve fibers and respond to the degree of stretching by blood pressure of the walls of blood vessels and the heart by changing the number of nerve impulses. The higher the pressure, the higher the frequency of nerve impulses is generated in the nerve endings that form baroreceptors. From receptors to afferent nerve fibers IX and X pairs of cranial nerves streams of signals about the current value of blood pressure are transmitted to the nerve centers that regulate blood circulation. They receive information from chemoreceptors that control the tension of blood gases, from receptors in muscles, joints, tendons, as well as from exteroceptors. The activity of neurons in the centers that regulate blood pressure and blood flow also depends on the influence on them higher departments brain.

One of the important functions of these centers is the formation of the level specified for regulation (set point) arterial blood pressure. Based on a comparison of information about the magnitude of the current pressure entering the centers with its specified level for regulation, the nerve centers form a flow of signals transmitted to the effector organs. By changing their functional activity, you can directly influence the level of arterial blood pressure, adapting its value to the current needs of the body.

Effector organs include: the heart, through the influence on the pumping function of which (stroke volume, heart rate, IOC), it is possible to influence the level of blood pressure; smooth myocytes of the vascular wall, through the influence on the tone of which it is possible to change the resistance of blood vessels to blood flow, blood pressure and blood flow in organs and tissues; kidneys, through influencing the processes of excretion and reabsorption of water in which it is possible to change the volume of circulating blood (CBV) and its pressure; blood depot, red Bone marrow, vessels of the microvasculature, in which, through the deposition, formation and destruction of red blood cells, the processes of filtration and reabsorption, it is possible to influence the bcc, its viscosity and pressure. Through the influence on these effector organs and tissues, the body's mechanisms of neurohumoral regulation (MHRR) can change blood pressure in accordance with the level set in the central nervous system, adapting it to the needs of the body.

The functional system of blood circulation regulation has various mechanisms of influence on the functions of effector organs and tissues. Among them are the mechanisms of the autonomic nervous system, adrenal hormones, using which you can change the functioning of the heart, the lumen (resistance) of blood vessels and influence blood pressure instantly (in seconds). In the functional system, signaling molecules (hormones, vasoactive substances of the endothelium and other nature) are widely used to regulate blood circulation. Their release and effect on target cells (smooth myocytes, renal tubular epithelium, hematopoietic cells, etc.) require tens of minutes, and changes in the volume of blood volume and its viscosity may require a longer time. Therefore, according to the speed of implementation of the effect on blood pressure levels, mechanisms of rapid response, medium-term response, slow response and long-term influence on blood pressure are distinguished.

> Rapid response mechanisms And quick influence changes in blood pressure are realized through the reflex mechanisms of the autonomic nervous system (ANS). Principles of construction neural pathways ANS reflexes are discussed in the chapter on the autonomic nervous system.

Reflex reactions to changes in blood pressure levels can change the value of blood pressure in seconds and thereby change the speed of blood flow in the vessels and transcapillary exchange. Mechanisms of rapid response and reflex regulation of blood pressure are activated when there is a sharp change in blood pressure, a change in the gas composition of the blood, cerebral ischemia, or psychoemotional arousal.

Any reflex is initiated by sending receptor signals to the centers of the reflex. Places of accumulation of receptors that respond to one type of influence are usually called reflexogenic zones. It has already been briefly mentioned that receptors that perceive changes in blood pressure are called baroreceptors or stretch mechanoreceptors. They respond to fluctuations in blood pressure, causing greater or lesser stretching of the vessel walls, by changing the potential difference on the receptor membrane. The main number of baroreceptors is concentrated in the reflexogenic zones of large vessels and the heart. The most important of them for regulating blood pressure are the areas of the aortic arch and carotid sinus (the place where the common carotid artery branches into the internal and external carotid arteries). In these reflexogenic zones, not only baroreceptors are concentrated, but also chemoreceptors that perceive changes in the tension of CO 2 (pCO 2) and 0 2 (p0 2) in the arterial blood.

Afferent nerve impulses arising in the receptor nerve endings are carried to the medulla oblongata. From the receptors of the aortic arch, they go along the left depressor nerve, which in humans passes through the trunk of the vagus nerve (the right depressor nerve carries impulses from receptors located at the beginning of the brachiocephalic arterial trunk). Afferent impulses from the carotid sinus receptors are carried out as part of a branch of the sinocarotid nerve, also called Hering's nerve(as part of the glossopharyngeal nerve).

Vascular baroreceptors respond by changing the frequency of generation of nerve impulses to normal fluctuations in blood pressure levels. During diastole, when the pressure decreases (up to 60-80 mm Hg), the number of generated nerve impulses decreases, and with each ventricular systole, when the blood pressure in the aorta and arteries increases (up to 120-140 mm Hg), the frequency the impulses sent by these receptors to the medulla oblongata increase. The increase in afferent impulses progressively increases if blood pressure increases above normal. Afferent impulses from baroreceptors enter the neurons of the depressor section of the circulatory center of the medulla oblongata and increase their activity. There are reciprocal relationships between the neurons of the depressor and pressor sections of this center, therefore, when the activity of the neurons of the depressor section increases, the activity of the neurons of the pressor section of the vasomotor center is inhibited.

Neurons of the pressor region send axons to preganglionic neurons of the sympathetic nervous system spinal cord which innervate blood vessels through ganglionic neurons. As a result of a decrease in the flow of nerve impulses to preganglionic neurons, their tone decreases and the frequency of nerve impulses sent by them to the ganglion neurons and further to the vessels decreases. The amount of norepinephrine released from postganglionic nerve fibers decreases, the vessels dilate and blood pressure decreases (Fig. 1.18).

In parallel with the initiation of reflex dilation of arterial vessels to increase blood pressure, rapid reflex inhibition of the pumping function develops

Rice. 1.18. Influence of the sympathetic nervous system on the lumen of arterial vessels muscular type and blood pressure with its low (left) and high (right) heart tone. It occurs due to the sending of an increased flow of signals from baroreceptors along the afferent fibers of the vagus nerve to the neurons of the nerve nucleus. At the same time, the activity of the latter increases, and the flow of efferent signals sent along the fibers of the vagus nerve to the pacemaker cells of the heart and the atrial myocardium increases. The frequency and strength of heart contractions decrease, which leads to a decrease in IOC and helps reduce increased blood pressure. Thus, baroreceptors monitor not only changes in blood pressure, their signals are used to regulate pressure when it deviates from the normal level. These receptors and the reflexes they produce are sometimes called “blood pressure regulators.”

A different direction of the reflex reaction occurs in response to a decrease in blood pressure. It is manifested by vasoconstriction and increased heart function, which contribute to an increase in blood pressure.

Reflex vasoconstriction and increased heart function are observed with increased activity of chemoreceptors located in the aortic and carotid bodies. These receptors are already active at normal voltage in the arterial layer pC0 2 and p0 2. From them there is a constant flow of afferent signals to the neurons of the pressor section of the vasomotor center and to the neurons of the respiratory center of the medulla oblongata. The activity of 0 2 receptors increases with a decrease in p0 2 in arterial blood plasma, and the activity of CO 2 receptors increases with an increase in pCO 2 and a decrease in pH. This is accompanied by an increase in the sending of signals to the medulla oblongata, an increase in the activity of neurons in the pressor region and the activity of preganglionic neurons in the sympathetic division of the ANS in the spinal cord, which send efferent signals of higher frequency to the blood vessels and heart. The blood vessels narrow, the heart increases the frequency and strength of contractions, which leads to an increase in blood pressure.

The described reflex reactions of blood circulation are called own since their receptor and effector links belong to the structures of the cardiovascular system. If reflex influences on blood circulation are carried out from a reflexogenic zone located outside the heart and blood vessels, then such reflexes are called conjugated. A number of them (reflexes of Goltz, Danini - Aschner, etc.) are discussed in the chapter devoted to the regulation of cardiac activity. Reflex

Goltz is manifested by the fact that when you hold your breath in the position of deep inspiration and increase the pressure in abdominal cavity there is a decrease in heart rate. If such a decrease exceeds 6 contractions per minute, then this indicates increased excitability of the neurons of the vagus nerve nuclei. Effects on skin receptors can cause both inhibition and activation of cardiac activity. For example, when cold receptors in the skin in the abdominal area are irritated, the heart rate decreases.

During psychoemotional arousal, due to stimulating descending influences, neurons of the pressor section of the vasomotor center are activated, which leads to activation of neurons of the sympathetic nervous system and an increase in blood pressure. A similar reaction develops with ischemia of the central nervous system.

The neuro-reflex effect on blood pressure is achieved by the influence of norepinephrine and adrenaline through stimulation of adrenergic receptors and intracellular mechanisms of vascular smooth myocytes and cardiac myocytes.

Centers for circulatory regulation located in the spinal cord, medulla oblongata, hypothalamus and cerebral cortex. Many other structures of the central nervous system can influence blood pressure levels and heart function. These influences are realized primarily through their connections with the centers of the medulla oblongata and spinal cord.

TO spinal cord centers include preganglionic neurons of the sympathetic division of the ANS ( side horns C8-L3 segments), which send axons to ganglion neurons located in the prevertebral and paravertebral ganglia and directly innervating vascular smooth myocytes, as well as preganglionic neurons of the lateral horns (Thl-Th3), which regulate heart function through modulation of the activity of ganglion neurons mainly in the cervical ganglia ).

The neurons of the sympathetic nervous system of the lateral horns of the spinal cord are effector neurons. Through them the centers of regulation of blood circulation of the medulla oblongata and more high levels The central nervous system (hypothalamus, raphe nucleus, pons, periaqueductal gray matter of the midbrain) affects vascular tone and heart function. At the same time, experimental and clinical observations indicate that these neurons reflexively regulate blood flow in certain areas of the vascular bed, and also independently regulate blood pressure levels when the connection between the spinal cord and the brain is disrupted.

The possibility of regulating blood pressure by neurons of the sympathetic nervous system of the spinal cord is based on the fact that their tone is determined not only by the influx of signals from the overlying parts of the central nervous system, but also by the influx of nerve impulses to them from the mechano-, chemo-, thermo- and pain receptors of blood vessels, internal organs, skin, musculoskeletal system. When the influx of afferent nerve impulses to these neurons changes, their tone also changes, which is manifested by a reflex narrowing or dilation of blood vessels and an increase or decrease in blood pressure. Such reflex effects on the lumen of blood vessels from the spinal centers of blood circulation regulation provide a relatively rapid reflex increase or restoration of blood pressure after its decrease in conditions of rupture of connections between the spinal cord and the brain.

Located in the medulla oblongata vasomotor center, discovered by F.V. Ovsyannikov. It is part of the cardiovascular, or cardiovascular, center of the central nervous system (see reflex regulation of the heart in this chapter). In particular, in the reticular formation of the medulla oblongata, together with the neurons that control vascular tone, the neurons of the center for regulating cardiac activity are located. The vasomotor center is represented by two sections: the pressor, the activation of neurons of which causes vasoconstriction and an increase in blood pressure, and the depressor, the activation of neurons of which leads to a decrease in blood pressure.

As can be seen from Fig. 1.19, neurons of the pressor and depressor divisions receive different afferent signals and are differently connected to effector neurons. Neurons of the pressor region receive afferent signals along the fibers of the IX and X cranial nerves from vascular chemoreceptors, signals from chemoreceptors of the medulla oblongata, from neurons of the respiratory center, neurons of the hypothalamus, and also from neurons of the cerebral cortex.

Axons of neurons of the pressor region form excitatory synapses on the bodies of preganglionic sympathetic neurons of the thoracolumbar region of the spinal cord. With increased activity, the neurons of the pressor region send an increased flow of efferent nerve impulses to the neurons

Rice. 1.19.

sympathetic part of the spinal cord, increasing their activity and thereby the activity of ganglion neurons that innervate the heart and blood vessels (Fig. 1.20).

Preganglonar neurons of the spinal centers, even under resting conditions, have tonic activity and constantly send signals to ganglion neurons, which, in turn, send rare (frequency 1-3 Hz) nerve impulses to the vessels. One of the reasons for the generation of these nerve impulses is the arrival of descending signals to the neurons of the spinal centers from some of the pressor neurons.

Rice. 1.20.

departments with spontaneous, pacemaker-like activity. Thus, the spontaneous activity of neurons of the pressor region, preganglionic spinal centers for circulatory regulation and ganglion neurons are, under resting conditions, a source of tonic activity of sympathetic nerves, which have a vasoconstrictor effect on the vessels.

An increase in the activity of preganglionic neurons, caused by an increase in the influx of signals from the pressor department, has a stimulating effect on the work of the heart, the tone of arterial and venous vessels. In addition, activated neurons of the pressor region are able to inhibit the activity of neurons of the depressor region.

Individual pools of pressor neurons may have stronger effects on certain areas of the vascular bed. Thus, the excitation of some of them leads to a greater constriction of the vessels of the kidneys, while the excitation of others leads to a significant constriction of the blood vessels gastrointestinal tract and less vasoconstriction of skeletal muscles. Inhibition of the activity of neurons in the pressor region leads to a decrease in blood pressure due to the elimination of the vasoconstrictor effect, suppression or loss of the reflex stimulating effect of the sympathetic nervous system on the work of the heart when chemo- and baroreceptors are irritated.

Neurons of the depressor section of the vasomotor center of the medulla oblongata receive afferent signals along the fibers of the IX and X cranial nerves from the baroreceptors of the aorta, blood vessels, heart, as well as from neurons of the hypothalamic center for circulatory regulation, from neurons of the limbic system, and cerebral cortex. When their activity increases, they inhibit the activity of neurons in the pressor region and can, through inhibitory synapses, reduce or eliminate the activity of preganglionic neurons in the sympathetic region of the spinal cord.

There is a reciprocal relationship between the depressor and pressor sections. If, under the influence of afferent signals, the depressor section is excited, this leads to inhibition of the activity of the pressor section and the latter sends a lower frequency of efferent nerve impulses to the neurons of the spinal cord, causing less vasoconstriction. A decrease in the activity of spinal neurons can lead to the cessation of their sending of efferent nerve impulses to the vessels, causing the dilation of blood vessels to the lumen, determined by the level of basal tone of the smooth myocytes of their wall. When blood vessels dilate, blood flow through them increases, the OPS value decreases and blood pressure decreases.

IN hypothalamus There are also groups of neurons, the activation of which causes changes in the functioning of the heart, the reaction of blood vessels and affects blood pressure. These influences can be realized by the hypothalamic centers through changes in the tone of the ANS. Let us recall that an increase in the activity of the neural centers of the anterior hypothalamus is accompanied by an increase in tone parasympathetic division ANS, decreased pumping function of the heart and blood pressure. An increase in neural activity in the posterior hypothalamus is accompanied by an increase in the tone of the sympathetic division of the ANS, increased heart function and an increase in blood pressure.

Hypothalamic centers for circulatory regulation are of leading importance in the mechanisms of integration of the functions of the cardiovascular system and other vegetative functions organism. It is known that the cardiovascular system is one of the most important in the mechanisms of thermoregulation, and its active use in the processes of thermoregulation, it is initiated by the hypothalamic centers for regulating body temperature (see “Thermoregulation”). The circulatory system actively responds to changes in blood glucose levels and blood osmotic pressure, to which hypothalamic neurons are highly sensitive. In response to a decrease in blood glucose levels, the tone of the sympathetic nervous system increases, and with an increase in the osmotic pressure of the blood, vosopressin is formed in the hypothalamus, a hormone that has a constricting effect on blood vessels. The hypothalamus influences blood circulation through other hormones, the secretion of which is controlled by the sympathetic division of the ANS (adrenaline, norepinephrine) and hypothalamic liberins and statins (corticosteroids, sex hormones).

Structures of the limbic system, being part of the emotiogenic areas of the brain, through connections with the hypothalamic centers for circulatory regulation, they can have a pronounced effect on the functioning of the heart, vascular tone and blood pressure. An example of such an influence is the well-known increase in heart rate, stroke volume and blood pressure during excitement, dissatisfaction, anger, and emotional reactions of other origins.

Cerebral cortex also affects the functioning of the heart, vascular tone and blood pressure through connections with the hypothalamus and neurons of the cardiovascular center of the medulla oblongata. The cerebral cortex can influence blood circulation by participating in the regulation of the release of adrenal hormones into the blood. Local irritation of the motor cortex causes an increase in blood flow in the muscles in which the contraction is initiated. Important reflex mechanisms play. It is known that due to the formation of conditioned vasomotor reflexes, changes in blood circulation can be observed in the pre-start state, even before the onset of muscle contraction, when the pumping function of the heart increases, blood pressure increases, and the intensity of blood flow in the muscles increases. Such changes in blood circulation prepare the body to perform physical and emotional stress.

> Medium-term response mechanisms Changes in blood pressure begin to act after tens of minutes and hours.

Among the mechanisms of medium-term response, an important role belongs to the mechanisms of the kidney. So, with a prolonged decrease in blood pressure and thereby a decrease in blood flow through the kidney, the cells of its juxtaglomerular apparatus react with the release of the enzyme renin into the blood, under the action of which angiotensin I (AT I) is formed from a 2 - globulin of the blood plasma, and from it under the influence of angiotensin-converting enzyme ( ACE) is formed by AT II. AT II causes contraction of smooth muscle cells of the vascular wall and has a strong vasoconstrictive effect on arteries and veins, increases the return of venous blood to the heart, SV and increases blood pressure. An increase in the level of renin in the blood is also observed with an increase in the tone of the sympathetic section of the ANS and a decrease in the level of Na + ions in the blood.

The mechanisms of medium-term response to changes in blood pressure include changes in the transcapillary exchange of water between blood and tissues. With a prolonged increase in blood pressure, the filtration of water from the blood into the tissues increases. Due to the release of fluid from the vascular bed, the BCC decreases, which helps to lower blood pressure. Reverse phenomena can develop with a decrease in blood pressure. The result of excessive filtration of water in the tissue with an increase in blood pressure may be the development of tissue edema, observed in patients with arterial hypertension.

Among the medium-term mechanisms of blood pressure regulation include mechanisms associated with the response of smooth myocytes of the vascular wall to a long-term increase in blood pressure. With a prolonged increase in blood pressure, vascular stress relaxation is observed - relaxation of smooth myocytes, which contributes to vasodilation, a decrease in peripheral resistance to blood flow and a decrease in blood pressure.

> Slow response mechanisms changes in blood pressure and violation of its regulation begin to act days and months after its change. The most important of them are the renal mechanisms of blood pressure regulation, realized through changes in the BCC. A change in BCC is achieved through the influence of signaling molecules of the renin-angiotensin H-aldosterone system, natriuretic peptide (NUP) and antidiuretic hormone (ADH) on the processes of filtration and reabsorption of Na + ions, filtration and reabsorption of water and urine excretion.

With high blood pressure, the excretion of fluid in the urine increases. This leads to a gradual decrease in the amount of fluid in the body, a decrease in bcc, a decrease in venous return of blood to the heart, a decrease in SV, IOC and blood pressure. The main role in the regulation of renal diuresis (the volume of urine excreted) is played by ADH, aldosterone and NUP. With an increase in the content of ADH and aldosterone in the blood, the kidneys increase the retention of water and sodium in the body, contributing to an increase in blood pressure. Under the influence of NUP, the excretion of sodium and water in the urine increases, diuresis increases, and blood volume decreases, which is accompanied by a decrease in blood pressure.

The level of ADH in the blood and its formation in the hypothalamus depend on the volume of blood volume, the value of blood pressure, its osmotic pressure and the level of AT II in the blood. Thus, the level of ADH in the blood increases with a decrease in blood volume, a decrease in blood pressure, an increase in blood osmotic pressure, and an increase in the level of AT II in the blood. In addition, the release of ADH into the blood by the pituitary gland is influenced by the influx of afferent nerve impulses from baroreceptors, atrial stretch receptors and large veins into the vasomotor center of the medulla oblongata and the hypothalamus. With an increase in the influx of signals in response to the distension of the atria and large veins by the blood, a decrease in the release of ADH into the blood, a decrease in water reabsorption in the kidneys, an increase in diuresis and a decrease in volume are observed.

The level of aldosterone in the blood is controlled by the action of AT II, ​​ACTH, Na + and K + ions on the cells of the glomerular layer of the adrenal glands. Aldosterone stimulates the synthesis of sodium transport protein and increases sodium reabsorption in the renal tubules. Aldosterone thereby reduces the excretion of water by the kidneys, promotes an increase in BCC and an increase in blood pressure, an increase in blood pressure by increasing the sensitivity of vascular smooth muscle cells to the action of vasoconstrictors (adrenaline, angiotensin).

The main amount of NUP is formed in the atrial myocardium (for which reason it is also called atriopeptide). Its release into the blood increases with increasing atrial stretch, for example, under conditions of increased blood volume and venous return. Natriuretic peptide helps reduce blood pressure by reducing the reabsorption of Na + ions in the renal tubules, increasing the excretion of Na + ions and water in the urine and reducing the volume of blood volume. In addition, NUP has a dilating effect on blood vessels, blocking calcium channels of smooth myocytes of the vascular wall, reducing the activity of the renin-angiotensin system and the formation of endothelins. These effects of NUP are accompanied by a decrease in the resistance to blood flow and lead to a decrease in blood pressure.

After we have learned the classification and normal numbers of blood pressure, one way or another it is necessary to return to the issues of circulatory physiology. Blood pressure healthy person, despite significant fluctuations depending on physical and emotional stress, as a rule, is maintained at a relatively stable level. This is facilitated by complex mechanisms nervous and humoral regulation, which strive to return blood pressure to its original level after the end of the action of provoking factors. Maintaining blood pressure at a constant level is ensured by the coordinated functioning of the nervous and endocrine systems, as well as the kidneys.

All known pressor (increasing pressure) systems, depending on the duration of the effect, are divided into systems:

• rapid response (baroreceptors of the sinocarotid zone, chemoreceptors, sympathoadrenal system) - begins in the first seconds and lasts several hours;
• medium duration (renin-angiotensin) - turns on after a few hours, after which its activity can be either increased or decreased;
• long-acting (sodium-volume-dependent and aldosterone) - can act for a long time.

All mechanisms are, to a certain extent, involved in regulating the activity of the circulatory system, both under natural loads and under stress. The activity of internal organs - the brain, heart and others - is highly dependent on their blood supply, for which it is necessary to maintain blood pressure in the optimal range. That is, the degree of increase in blood pressure and the rate of its normalization must be adequate to the degree of load.

When blood pressure is too low, a person is prone to fainting and loss of consciousness. This is due to insufficient blood supply to the brain. In the human body, there are several systems for monitoring and stabilizing blood pressure, which mutually support each other. The nervous mechanisms are represented by the autonomic nervous system, the regulatory centers of which are located in the subcortical areas of the brain and are closely connected with the so-called vasomotor center of the medulla oblongata.

These centers receive the necessary information about the state of the system from a kind of sensors - baroreceptors located in the walls of large arteries. Baroreceptors are located primarily in the walls of the aorta and carotid arteries, which supply blood to the brain. They respond not only to the value of blood pressure, but also to the rate of its increase and the amplitude of pulse pressure. Pulse pressure is a calculated indicator that means the difference between systolic and diastolic blood pressure. Information from the receptors travels along the nerve trunks to the vasomotor center. This center controls arterial and venous tone, as well as the strength and frequency of heart contractions.

When deviating from standard values, for example, when blood pressure decreases, the cells of the center send a command to the sympathetic neurons, and the tone of the arteries increases. The baroreceptor system is one of the fast-acting regulatory mechanisms; its effect is manifested within a few seconds. The power of regulatory influences on the heart is so great that severe irritation baroreceptor zone, for example, with a sharp blow to the area of ​​the carotid arteries, it can cause short-term cardiac arrest and loss of consciousness due to sharp fall Blood pressure in the vessels of the brain. The peculiarity of baroreceptors is their adaptation to a certain level and range of blood pressure fluctuations. The phenomenon of adaptation is that receptors respond to changes in the usual pressure range less strongly than to changes of the same magnitude in an unusual blood pressure range. Therefore, if for any reason the blood pressure level remains persistently elevated, the baroreceptors adapt to it and their level of activation decreases ( this level Blood pressure is already considered normal). This kind of adaptation occurs when arterial hypertension, and caused by the use of medications sharp a decrease in blood pressure will already be perceived by baroreceptors as dangerous decline AD with subsequent intensification of counteraction to this process. When the baroreceptor system is artificially switched off, the range of blood pressure fluctuations during the day increases significantly, although on average it remains in the normal range (due to the presence of other regulatory mechanisms). In particular, the action of the mechanism that monitors the sufficient supply of brain cells with oxygen is realized just as quickly.

For this purpose, there are special sensors in the vessels of the brain that are sensitive to the oxygen tension in arterial blood - chemoreceptors. Since the most common reason for a decrease in oxygen tension is a decrease in blood flow due to a decrease in blood pressure, the signal from the chemoreceptors goes to the higher sympathetic centers, which can increase the tone of the arteries and also stimulate the heart. Thanks to this, blood pressure is restored to the level necessary to supply blood to brain cells.

The third mechanism, sensitive to changes in blood pressure, acts more slowly (over several minutes) - the renal mechanism. Its existence is determined by the operating conditions of the kidneys, which require maintaining stable pressure in the renal arteries for normal blood filtration. For this purpose, the so-called juxtaglomerular apparatus (JGA) functions in the kidneys. When pulse pressure decreases due to one reason or another, ischemia of the JGA occurs and its cells produce their hormone - renin, which is converted in the blood into angiotensin-1, which in turn, thanks to the angiotensin-converting enzyme (ACE), is converted into angiotensin-2, which has a strong vasoconstrictor effect, and blood pressure increases.

The renin-angiotensin system (RAS) regulation does not respond as quickly and accurately as the nervous system, and therefore even a short-term decrease in blood pressure can trigger the formation of a significant amount of angiotensin-2 and thereby cause a sustained increase in arterial tone. In this regard, a significant place in the treatment of diseases of the cardiovascular system belongs to drugs that reduce the activity of the enzyme that converts angiotensin-1 into angiotensin-2. The latter, acting on the so-called type 1 angiotensin receptors, has many biological effects.

• Peripheral vasoconstriction
• Aldosterone release
• Synthesis and release of catecholamines
• Control of glomerular circulation
• Direct antinatriuretic effect
• Stimulation of hypertrophy of vascular smooth muscle cells
• Stimulation of cardiomyocyte hypertrophy
• Stimulation of connective tissue development (fibrosis)

One of them is the release of aldosterone by the adrenal cortex. The function of this hormone is to reduce the excretion of sodium and water in the urine (antinatriuretic effect) and, accordingly, to retain them in the body, that is, to increase circulating blood volume (CBV), which also increases blood pressure.

Renin-angiotensin system (RAS)

The RAS, the most important among the humoral endocrine systems regulating blood pressure, influences the two main determinants of blood pressure—peripheral resistance and circulating blood volume. There are two types of this system: plasma (systemic) and tissue. Renin is secreted by the UGA of the kidneys in response to a decrease in pressure in the afferent arteriole of the glomeruli of the kidneys, as well as a decrease in sodium concentration in the blood.

ACE plays the main role in the formation of angiotensin 2 from angiotensin 1; there is another, independent pathway for the formation of angiotensin 2 - the non-circulating “local” or tissue renin-angiotensin paracrine system. It is found in the myocardium, kidneys, vascular endothelium, adrenal glands and nerve ganglia and is involved in the regulation of regional blood flow. The mechanism of formation of angiotensin 2 in this case is associated with the action of the tissue enzyme - chymase. As a result, efficiency may decrease ACE inhibitors, which do not affect this mechanism of angiotensin 2 formation. It should also be noted that the level of activation of the circulating RAS does not have a direct connection with an increase in blood pressure. In many patients (especially the elderly), plasma renin and angiotensin 2 levels are quite low.

Why, after all, does hypertension occur?

In order to understand this, you need to imagine that in the human body there is a kind of scale on one side of which there are pressor (that is, increasing blood pressure) factors, on the other - depressor (lowering blood pressure).

When pressor factors outweigh, pressure increases; when depressor factors outweigh, pressure decreases. And normally, in humans, these scales are in dynamic equilibrium, due to which the pressure is maintained at a relatively constant level.

What is the role of adrenaline and norepinephrine in the development of arterial hypertension?

The greatest importance in the pathogenesis of arterial hypertension is given to humoral factors. Has powerful direct pressor and vasoconstrictor activity catecholamines - adrenaline and norepinephrine, which are produced mainly in medulla adrenal glands. They are also neurotransmitters of the sympathetic division of the autonomic nervous system. Norepinephrine acts on the so-called alpha-adrenergic receptors and acts for quite a long time. Mainly peripheral arterioles narrow, which is accompanied by an increase in both systolic and diastolic blood pressure. Adrenaline, stimulating alpha and beta adrenergic receptors (b1 - cardiac muscle and b2 - bronchi), intensively but briefly increases blood pressure, increases blood sugar, increases tissue metabolism and the body's need for oxygen, and leads to an acceleration of heart contractions.

The effect of table salt on blood pressure

Kitchen or table salt in excess amounts increases the volume of extracellular and intracellular fluid, causes swelling of the artery walls, thereby contributing to the narrowing of their lumen. Increases the sensitivity of smooth muscles to pressor substances and causes an increase in total peripheral vascular resistance (TPVR).

What are the current hypotheses for the occurrence of arterial hypertension?

Currently, this point of view is accepted - the reason for the development of the primary (essential) is the complex influence of various factors, which are listed below.

Unmodifiable:

• age (2/3 of people over 55 years of age have hypertension, and if blood pressure is normal, the probability of developing it in the future is 90%)
• hereditary predisposition (up to 40% of cases of hypertension)
• intrauterine development (low birth weight). In addition to the increased risk of developing hypertension, there is also a risk of metabolic abnormalities associated with hypertension: insulin resistance, diabetes mellitus, hyperlipidemia, abdominal type obesity.

Modifiable lifestyle factors (80% of hypertension is associated with these factors):

• smoking,
• unhealthy diet (overeating, low potassium content, high salt and animal fats, low dairy products, vegetables and fruits),
• overweight and obesity (body mass index more than 25 kg/m2, central type of obesity - waist size in men over 102 cm, among women more than 88 cm),
• psychosocial factors (moral and psychological climate at work and at home),
• high level of stress,
• alcohol abuse,
• low level of physical activity.

Blood pressure is maintained at the required operating level with the help of reflex control mechanisms operating on the basis of the feedback principle.

 Baroreceptor reflex. One of the well-known neural mechanisms of blood pressure control is the baroreceptor reflex. Baroreceptors are present in the wall of almost all large arteries in the chest and neck, especially in the carotid sinus and in the wall of the aortic arch. Baroreceptors of the carotid sinus (see Fig. 25–10) and aortic arch do not respond to blood pressure ranging from 0 to 60–80 mm Hg. An increase in pressure above this level causes a response that progressively increases and reaches a maximum at blood pressure of about 180 mm Hg. Normal blood pressure (its systolic level) ranges from 110–120 mm Hg. Small deviations from this level increase the excitation of baroreceptors. Baroreceptors respond to changes in blood pressure very quickly: the impulse frequency increases during systole and decreases just as quickly during diastole, which occurs within a fraction of a second. Thus, baroreceptors are more sensitive to changes in pressure than to stable levels.

 Increased impulses from baroreceptors, caused by a rise in blood pressure, enters the medulla oblongata, inhibits the vasoconstrictor center of the medulla oblongata and stimulates the vagus nerve center. As a result, the lumen of the arterioles expands, and the frequency and strength of heart contractions decreases. In other words, excitation of baroreceptors reflexively leads to a decrease in blood pressure due to a decrease in peripheral resistance and cardiac output.

 Low blood pressure has the opposite effect, which leads to its reflex increase to a normal level. A decrease in pressure in the area of ​​the carotid sinus and aortic arch inactivates baroreceptors, and they cease to have an inhibitory effect on the vasomotor center. As a result, the latter is activated and causes an increase in blood pressure.

 Orthostatic collapse. The baroreceptor reflex takes part in maintaining blood pressure when changing from a horizontal to a vertical position. Immediately after assuming a vertical position, blood pressure in the head and upper torso decreases, which can cause loss of consciousness (which happens in some cases with insufficiency of the baroreceptor reflex - this condition is called orthostatic syncope). The drop in pressure in the baroreceptor area immediately activates a reflex that excites the sympathetic system and minimizes the decrease in pressure in the upper torso and head.

 Chemoreceptors of the carotid sinus and aorta. Chemoreceptors - chemosensitive cells that respond to a lack of oxygen, excess carbon dioxide and hydrogen ions - are located in the carotid bodies and in the aortic bodies. Chemoreceptor nerve fibers from the corpuscles, together with baroreceptor fibers, go to the vasomotor center of the medulla oblongata. When blood pressure decreases below a critical level, chemoreceptors are stimulated, since the decrease in blood flow reduces the O 2 content and increases the concentration of CO 2 and H +. Thus, impulses from chemoreceptors excite the vasomotor center and contribute to an increase in blood pressure.

 Reflexes with pulmonary artery and atria. There are stretch receptors (low pressure receptors) in the wall of both atria and the pulmonary artery. Low pressure receptors perceive changes in volume that occur simultaneously with changes in blood pressure. Excitation of these receptors causes reflexes in parallel with baroreceptor reflexes.

 Reflexes from the atria,kidney activating. Stretching of the atria causes a reflex expansion of the afferent (afferent) arterioles in the glomeruli of the kidneys. At the same time, a signal travels from the atrium to the hypothalamus, reducing the secretion of ADH. The combination of two effects - an increase in glomerular filtration and a decrease in fluid reabsorption - helps to reduce blood volume and return it to normal level.

 Atrial reflex that controls heart rate. An increase in pressure in the right atrium causes a reflex increase in heart rate (Bainbridge reflex). Atrial stretch receptors, which cause the Bainbridge reflex, transmit afferent signals through the vagus nerve to the medulla oblongata. The excitation then returns back to the heart through the sympathetic pathways, increasing the frequency and force of heart contractions. This reflex prevents the veins, atria and lungs from overflowing with blood.

 Direct effects on the vasomotor center. If blood circulation in the brainstem region decreases, causing cerebral ischemia, then the excitability of the neurons of the vasomotor center increases significantly, leading to a maximum increase in systemic blood pressure. This effect is caused by the local accumulation of CO 2, lactic acid and other acidic substances and their stimulating effect on the sympathetic part of the vasomotor center. The ischemic response of the central nervous system to blood circulation is unusually large: within 10 minutes, average blood pressure can sometimes rise to 250 mm Hg. The ischemic response of the central nervous system is one of the most powerful activators of the sympathetic vasoconstrictor system. This mechanism occurs when blood pressure drops to 60 mmHg. and lower, which happens with large blood loss, circulatory shock, collapse. This is a reaction of the life-saving pressure control system, preventing a further drop in blood pressure to lethal levels.

 ReflexCushing(Cushing reaction) - ischemic reaction of the central nervous system in response to increased intracranial pressure. If intracranial pressure increases and becomes equal to blood pressure, then the arteries in the cranial cavity are compressed and ischemia occurs. Ischemia causes an increase in blood pressure, and blood flows back into the brain, overcoming the compressive effect of increased intracranial pressure. Simultaneously with the increase in pressure, the heart rhythm and breathing rate become less frequent due to the stimulation of the vagus nerve center.

 Renin-angiotensin system discussed in Chapter 29.

In order for the mechanisms that regulate blood pressure to adequately respond to the needs of the body, they must receive information about these needs.

This function is performed by chemoreceptors. Chemoreceptors respond to a lack of oxygen in the blood, an excess of carbon dioxide and hydrogen ions, and a shift in the blood reaction (blood pH) to the acidic side. Chemoreceptors are found throughout the vascular system. There are especially many of these cells in the common carotid artery and in the aorta.

A lack of oxygen in the blood, an excess of carbon dioxide and hydrogen ions, and a shift in blood pH to the acidic side excite chemoreceptors. Impulses from chemoreceptors travel along nerve fibers to the vasomotor center of the brain (VMC). SDC consists of nerve cells(neurons) that regulate vascular tone, strength, heart rate, volume of circulating blood, that is, blood pressure. The SDC neurons exert their influence on vascular tone, the strength and frequency of heart contractions, and the volume of circulating blood through the neurons of the sympathetic and parasympathetic autonomic nervous system (ANS), which directly affect vascular tone, the strength and frequency of heart contractions.

The SDC consists of pressor, depressor and sensory neurons. An increase in the excitation of pressor neurons increases the excitation (tone) of neurons sympathetic ANS and reduces the tone of the parasympathetic ANS. This leads to an increase in vascular tone (vascular spasm, reduction in the lumen of blood vessels), to an increase in the strength and frequency of heart contractions, that is, to an increase in blood pressure. Depressor neurons reduce the excitation of pressor neurons and, thus, indirectly contribute to vasodilation (decreasing vascular tone), reduce the strength and frequency of heart contractions, that is, lower blood pressure.

Sensory (sensitive) neurons, depending on the information received from the receptors, have an excitatory effect on the pressor or depressor neurons of the SDC.

The functional activity of pressor and depressor neurons is regulated not only by sensory neurons of the SDC, but also by other neurons of the brain. Indirectly through the hypothalamus, neurons of the motor zone of the cerebral cortex have an excitatory effect on pressor neurons.

Neurons of the cerebral cortex influence the SDC through neurons of the hypothalamic region.

Strong emotions: anger, fear, anxiety, excitement, great joy, grief can cause excitation of the pressor neurons of the SDC. Pressor neurons excite on their own if they are in a state of ischemia (a state of insufficient oxygen supply to them with the blood). In this case, blood pressure rises very quickly and very strongly. The fibers of the sympathetic ANS densely intertwine the vessels, the heart, and end with numerous branches in various organs and tissues of the body, including near cells called transducers. These cells, in response to an increase in the tone of the sympathetic ANS, begin to synthesize and release substances into the blood that affect the increase in blood pressure.

Transducers are:

• 1. Chromaffin cells of the adrenal medulla;
• 2. Juxt-glomerular cells of the kidneys;
• 3. Neurons of the hypothalamic supraoptic and paraventricular nuclei.

Chromaffin cells of the adrenal medulla.

These cells, with an increase in the tone of the sympathetic ANS, begin to synthesize and release hormones into the blood: adrenaline and norepinephrine. These hormones in the body have the same effects as the sympathetic ANS. In contrast to the influence of the sympathetic ANS system, the effects of adrenaline and norepinephrine in the adrenal glands are more prolonged and widespread.

Juxt-glomerular cells of the kidneys.

These cells, with an increase in the tone of the sympathetic ANS, as well as during renal ischemia (a state of insufficient supply of oxygen to the kidney tissues with the blood), begin to synthesize and release the proteolytic enzyme renin into the blood.

Renin in the blood breaks down another protein, angiotensinogen, to form the protein angiotensin 1. Another enzyme in the blood, ACE (Angiotensin Converting Enzyme), breaks down angiotensin 1 to form the protein angiotensin 2.

Angiotensin 2:

• - has a very strong and long-lasting vasoconstrictive effect on blood vessels. Angiotensin 2 realizes its effect on vessels through angiotensin receptors (AT);
• - stimulates the synthesis and release of aldosterone into the blood by the cells of the glomerular zone of the adrenal glands, which retains sodium, and, therefore, water in the body. This leads to: an increase in the volume of circulating blood, sodium retention in the body leads to the fact that sodium penetrates into the endothelial cells that cover blood vessels from the inside, carrying water with it inside the cell. Endothelial cells increase in volume. This leads to a narrowing of the lumen of the vessel. Reducing the lumen of the vessel increases its resistance. An increase in vascular resistance increases the strength of heart contractions. Sodium retention increases the sensitivity of angiotensin receptors to angiotensin 2. This accelerates and enhances the vasoconstrictor effect of angiotensin 2;
• - stimulates the cells of the hypothalamus to synthesize and secrete the antidiuretic hormone vasopressin into the blood and the adenohypophysis cells of adrenocorticotropic hormone (ACTH). ACTH stimulates the synthesis of glucocorticoids by the cells of the fascicular zone of the cortical layer of the adrenal glands. The largest biological effect has cortisol. Cortisol potentiates an increase in blood pressure.

All this in particular and in combination leads to an increase in blood pressure. The neurons of the hypothalamic supraoptic and paraventricular nuclei synthesize the antidiuretic hormone vasopressin. Through their processes, neurons release vasopressin into the posterior pituitary gland, from where it enters the bloodstream. Vasopressin has a vasoconstrictive effect, retains water in the body.

This leads to an increase in circulating blood volume and an increase in blood pressure. In addition, vasopressin enhances the vasoconstrictor effects of adrenaline, norepinephrine and angiotensin 2.

Information about the volume of circulating blood and the strength of heart contractions comes to the SDC from baroreceptors and low pressure receptors. Baroreceptors are branches of the processes of sensory neurons in the wall of arterial vessels. Baroreceptors convert stimulation from the stretching of the vessel wall into a nerve impulse. Baroreceptors are found throughout the vascular system.

Their greatest number is in the aortic arch and carotid sinus. Baroreceptors are stimulated by stretch. An increase in the force of heart contractions increases the stretching of the walls of arterial vessels at the locations of the baroreceptors. The excitation of baroreceptors increases in direct proportion to the increase in the strength of heart contractions. The impulse from them goes to the sensory neurons of the SDC. The sensory neurons of the SDC excite the depressor neurons of the SDC, which reduce the excitation of the pressor neurons of the SDC. This leads to a decrease in the tone of the sympathetic ANS and an increase in the tone of the parasympathetic ANS, which leads to a decrease in the strength and frequency of heart contractions, vasodilation, that is, to a decrease in blood pressure. On the contrary, the decrease in the strength of heart contractions is lower normal indicators reduces the excitation of baroreceptors, reduces impulses from them to the sensory neurons of the SDC. In response to this, the sensory neurons of the SDC excite the pressor neurons of the SDC.

This leads to an increase in the tone of the sympathetic ANS and a decrease in the tone of the parasympathetic ANS, which leads to an increase in the strength and frequency of heart contractions, vasoconstriction, that is, to an increase in blood pressure. In the walls of the atria and pulmonary artery there are low pressure receptors, which are excited when blood pressure decreases due to a decrease in the volume of circulating blood.

With blood loss, the volume of circulating blood decreases and blood pressure decreases. Excitation of baroreceptors decreases, and excitation of low pressure receptors increases.

This leads to an increase in blood pressure. As blood pressure approaches normal, excitation of baroreceptors increases, and excitation of low pressure receptors decreases.

This prevents blood pressure from increasing above normal. With blood loss, restoration of the volume of circulating blood is achieved by the transfer of blood from the depot (spleen, liver) into the bloodstream. Note: About 500 ml is deposited in the spleen. blood, and in the liver and in the vessels of the skin there is about 1 liter of blood.

The volume of circulating blood is controlled and maintained by the kidneys through the production of urine. When systolic blood pressure is less than 80 mm. rt. Art. urine is not formed at all, with normal blood pressure - normal urine formation, with increased blood pressure, urine is formed in direct proportion to more (hypertensive diuresis). At the same time, sodium excretion in the urine increases (hypertensive natriuresis), and water is also excreted along with sodium.

When the volume of circulating blood increases above normal, the load on the heart increases. In response to this, atrial cardiomycytes respond by synthesizing and releasing a protein into the blood - atrial natriuretic peptide (ANP), which increases the excretion of sodium and, therefore, water in the urine. The cells of the body can themselves regulate the supply of oxygen to them with the blood and nutrients.

Under conditions of hypoxia (ischemia, insufficient oxygen supply), cells secrete substances (for example, adenosine, nitric oxide NO, prostacyclin, carbon dioxide, adenosine phosphates, histamine, hydrogen ions (lactic acid), potassium ions, magnesium ions) that dilate the adjacent arterioles , thereby increasing the flow of blood, and, accordingly, oxygen and nutrients.

In the kidneys, for example, during ischemia, the cells of the renal medulla begin to synthesize and release kinins and prostaglandins into the blood, which have a vasodilating effect. As a result, the arterial vessels of the kidneys dilate, and the blood supply to the kidneys increases. Note: with excess salt intake from food, the synthesis of kinins and prostaglandins by kidney cells decreases.

Blood rushes primarily to where the arterioles are more dilated (to the place of least resistance). Chemoreceptors trigger a mechanism to increase blood pressure in order to speed up the delivery of oxygen and nutrients to cells, which the cells lack. As the ischemic state is resolved, the cells stop releasing substances that dilate adjacent arterioles, and the chemoreceptors stop stimulating an increase in blood pressure.