Mechanisms of nervous and humoral regulation of the heart and blood vessels. Reflex, nervous and humoral regulation of vascular tone Reflex and humoral regulation of blood vessels

The blood supply to the organs depends on the size of the lumen of the vessels, their tone and the amount of blood ejected into them by the heart. Therefore, when considering the regulation of vascular function, first of all we should talk about the mechanisms of maintaining vascular tone and the interaction of the heart and blood vessels.

Efferent innervation of blood vessels. Vascular lumen is mainly regulated by the sympathetic nervous system. Its nerves, independently or as part of mixed motor nerves, approach all arteries and arterioles and exert a vasoconstrictor effect (vasoconstriction). A clear demonstration of this influence is the experiments of Claude Bernard, carried out on the vessels of the rabbit ear. In these experiments, the sympathetic nerve was cut on one side of the rabbit's neck, after which redness of the ear of the operated side and a slight increase in its temperature were observed due to vasodilation and increased blood supply to the ear. Irritation of the peripheral end of the cut sympathetic nerve caused vasoconstriction and blanching of the ear.

Under the influence of the sympathetic nervous system, the vascular muscles are in a state of contraction - tonic tension.

Under natural conditions of the body's life, changes in the lumen of most vessels occur due to changes in the number of impulses traveling along the sympathetic nerves. The frequency of these pulses is low - approximately 1 pulse per second. Under the influence of reflex effects, their number can be increased or decreased. With an increase in the number of impulses, the tone of the vessels increases - they narrow. If the number of impulses decreases, the vessels dilate.

The parasympathetic nervous system has a vasodilatory effect ( vasodilation) only on the vessels of some organs. In particular, it dilates the blood vessels of the tongue, salivary glands and genitals. Only these three organs have double innervation: sympathetic (vasoconstrictor) and parasympathetic (vasodilator).

Characteristics of the vasomotor center. The neurons of the sympathetic nervous system, through the processes of which impulses travel to the vessels, are located in the lateral horns of the gray matter of the spinal cord. The level of activity of these neurons depends on the influences of the overlying parts of the central nervous system.

In 1871 F.V. Ovsyannikov showed that in the medulla oblongata there are neurons, under the influence of which vasoconstriction occurs. This center was named vasomotor. Its neurons are concentrated in the medulla oblongata at the bottom of the fourth ventricle near the nucleus of the vagus nerve.

In the vasomotor center, two sections are distinguished: pressor, or vasoconstrictor, and depressor, or vasodilator. When neurons are stimulated pressor center, vasoconstriction and increased blood pressure occur, and with irritation depressor - dilation of blood vessels and decrease in blood pressure. The neurons of the depressor center at the moment of their excitation cause a decrease in the tone of the pressor center, as a result of which the number of tonic impulses going to the vessels decreases and their dilation occurs.

Impulses from the vasoconstrictor center of the brain arrive at the lateral horns of the gray matter of the spinal cord, where the neurons of the sympathetic nervous system are located, forming the vasoconstrictor center of the spinal cord. From it, impulses travel through the fibers of the sympathetic nervous system to the muscles of the blood vessels and cause their contraction, resulting in a narrowing of the lumen of the blood vessels. Normally, the vasoconstrictor center is in good tone compared to the vasodilator center.

Reflex regulation of vascular tone. There are intrinsic and associated cardiovascular reflexes.

Own vascular reflexes are caused by signals from the receptors of the vessels themselves. The receptors located in the aortic arch and carotid sinus are of particular physiological importance. Impulses from these receptors take part in the regulation of blood pressure.

Conjugate vascular reflexes arise in other organs and systems and are manifested mainly by an increase in blood pressure. Thus, with mechanical or painful irritation of the skin, strong irritation of the visual and other receptors, a reflex narrowing of blood vessels occurs and an increase in blood pressure.

Humoral regulation of vascular tone. Chemical substances that affect the lumen of blood vessels are divided into vasoconstrictors and vasodilators.

Most powerful vasoconstrictor hormones of the adrenal medulla have an effect - adrenalin And norepinephrine, as well as the posterior lobe of the pituitary gland - vasopressin.

Adrenaline and norepinephrine constrict arteries and arterioles of the skin, abdominal organs and lungs, and vasopressin acts primarily on arterioles and capillaries.

Adrenaline is a biologically very active drug and acts in very small concentrations. 0.0002 mg of adrenaline per 1 kg of body weight is enough to cause vasoconstriction and an increase in blood pressure. The vasoconstrictor effect of adrenaline occurs in different ways. It acts directly on the vascular wall and reduces the membrane potential of its muscle fibers, increasing excitability and creating conditions for the rapid occurrence of excitation. Adrenaline affects the hypothalamus and leads to an increase in the flow of vasoconstrictor impulses and an increase in the amount of vasopressin released.

Humoral vasoconstrictor factors include serotonin, produced in the intestinal mucosa and in some areas of the brain. Serotonin is also formed during the breakdown of platelets. Serotonin constricts blood vessels and prevents bleeding from the affected vessel. In the second phase of blood coagulation, which develops after the formation of a blood clot, serotonin dilates blood vessels.

A special vasoconstrictor factor - renin, is formed in the kidneys, and in greater quantities, the lower the blood supply to the kidneys. For this reason, after partial compression of the renal arteries in animals, a persistent increase in blood pressure occurs due to narrowing of the arterioles. Renin is a proteolytic enzyme. Renin itself does not cause vasoconstriction, but, entering the blood, it breaks down plasma a2-globulin - angiotensinogen and turns it into a relatively inactive - angiotensin I. The latter, under the influence of a special angiotensin-converting enzyme, is converted into a very active vasoconstrictor substance - angiotensin II.

Under conditions of normal blood supply to the kidneys, a relatively small amount of renin is formed. It is produced in large quantities when blood pressure levels drop throughout the vascular system. If you lower a dog's blood pressure by bloodletting, the kidneys will release an increased amount of renin into the blood, which will help normalize blood pressure.

The discovery of renin and the mechanism of its vasoconstrictive action is of great clinical interest: it explained the cause of high blood pressure accompanying some kidney diseases (hypertension of renal origin).

Vasodilator Medulin, prostaglandins, bradykinin, acetylcholine, histamine have an effect.

Medulin produced in the medulla of the kidney and is a lipid.

Currently, it is known that a number of vasodilating substances are formed in many tissues of the body, called prostaglandins. This name was given because these substances were first found in the seminal fluid of men, and it was assumed that they were produced by the prostate gland. Prostaglandins are derivatives of unsaturated fatty acids.

An active vasodilator polypeptide was obtained from the submandibular, pancreas, lungs and some other organs Bradykinin. It causes relaxation of the smooth muscles of arterioles and lowers blood pressure levels. Bradykinin appears in the skin when exposed to heat and is one of the factors responsible for the dilation of blood vessels when heated. It is formed when one of the globulins in the blood plasma is broken down under the influence of an enzyme located in the tissues.

Vasodilators include acetylcholine(ACh), which is formed at the endings of parasympathetic nerves and sympathetic vasodilators. It is quickly destroyed in the blood, so its effect on blood vessels under physiological conditions is purely local.

It is also a vasodilator histamine, forming in the mucous membrane of the stomach and intestines, as well as in many other organs, in particular in the skin when it is irritated and in skeletal muscles during work. Histamine dilates arterioles and increases blood supply to capillaries. When 1-2 mg of histamine is injected into a cat's vein, despite the fact that the heart continues to work with the same force, the blood pressure level quickly drops due to a decrease in blood flow to the heart: a very large amount of the animal's blood becomes concentrated in the capillaries, mainly in the abdominal cavity. The decrease in blood pressure and circulatory disorders are similar to those that occur with large blood loss. They are accompanied by disruption of the central nervous system due to cerebrovascular accident. The combination of these phenomena is united by the concept of “shock”.

Severe disorders that occur in the body when large doses of histamine are administered are called histamine shock.

The increased formation and action of histamine explains the reaction of skin redness. This reaction is caused by various irritations, such as rubbing the skin, heat, and ultraviolet radiation.

Vasoconstrictor substances. These include the hormones of the adrenal medulla - adrenaline and norepinephrine, as well as the posterior lobe of the pituitary gland - vasopressin. Adrenaline and norepinephrine constrict arteries and arterioles of the skin, abdominal organs and lungs, and vasopressin acts primarily on arterioles and capillaries and affects blood vessels in very low concentrations.

Vasoconstrictor humoral factors include serotonin, produced in the intestinal mucosa and in some parts of the brain. It is also formed during the breakdown of platelets. The physiological significance of serotonin is that it constricts blood vessels and prevents bleeding from the affected vessel. In the second phase of blood coagulation, after the formation of a blood clot, serotonin dilates blood vessels.

Another vasoconstrictor factor, renin, is synthesized in the kidneys, and the lower their blood supply, the greater the quantity it is produced. Renin is a proteolytic enzyme. By itself, it does not cause vasoconstriction, but, entering the blood, it breaks down plasma ά 2 -globulin (angiotensinogen) and converts it into a relatively inactive angiotensin I, which, under the influence of the enzyme dipeptide carboxypeptidase (angiotensin convertase, angiotensin converting enzyme), transforms into a very active vasoconstrictor form - angiotensin II. The latter is quickly destroyed in the capillaries by angiotensinase. Under conditions of normal blood supply to the kidneys, a relatively small amount of renin is formed.

The discovery of renin and the mechanism of its vasoconstrictor action explained the cause of high blood pressure accompanying some kidney diseases.

Vasodilators. Many tissues of the body synthesize vasodilating substances called prostaglandins, which are derivatives of saturated fatty acids. Vasodilator peptides belonging to the group of kinins have been isolated from the submandibular glands, pancreas, lungs and some other organs. The most famous of them is bradykinin, which causes relaxation of the smooth muscles of arterioles and a decrease in blood pressure.

Vasodilating substances also include acetylcholine, which is produced in the endings of the parasympathetic nerves, and histamine, which is produced in the mucous membrane of the stomach and intestines, as well as in other organs, in particular in the skin and skeletal muscles. These substances cause dilation of arterioles and increased blood supply to capillaries.

In recent years, the important role of the endothelium of the vascular wall in the regulation of blood flow has been established. Endotheliocytes, under the influence of chemical stimuli brought by the blood (for example, NO), are capable of releasing substances that affect vascular tone and cause vasodilation.

The vessels of a number of organs and tissues have specific regulatory features, which are determined by the structure and function of this organ.

4.2.2. Pathophysiological changes in the cardiovascular system in critical conditions

Both experimental and clinical studies have demonstrated that various factors take part in the pathogenesis of disturbances in circulatory homeostasis in critical conditions: hypoxia, toxemia, redistribution of fluid across sectors with a general decrease in it, water-electrolyte, acid-base and energy imbalances, disorders hemorheology, etc. All of them cause a decrease in venous support, a decrease in myocardial contractility and cardiac performance, changes in vascular resistance, centralization of blood circulation, which ultimately leads to a deterioration in tissue perfusion. Despite the polyetiology of circulatory disorders in patients in critical conditions, there is a group of factors that directly determine the hemodynamic status of the patient, and a number of criteria that allow assessing this status. The main criterion for the functional state of the cardiovascular system is the magnitude of cardiac output. Its adequacy is ensured by:

a) venous return;

b) myocardial contractility;

c) peripheral resistance for the right and left ventricles;

d) heart rate;

e) condition of the heart valve apparatus.

Any circulatory disorders can be linked to the functional failure of the heart pump, if we consider cardiac output as the main indicator of its adequacy:

acute heart failure - decreased cardiac output with normal or increased venous return;

acute vascular insufficiency - impaired venous return due to an increase in the vascular bed;

acute blood circulation failure tion - decreased cardiac output regardless of the state of venous return.

Let's consider the most important factors influencing the magnitude of cardiac output.

Venous return - this is the volume of blood flowing through the vena cava into the right atrium. In normal clinical conditions, direct measurement of it is practically impossible, so indirect methods for its assessment are widely used, for example, research central venouslow pressure(CVD). The normal level of central venous pressure is approximately 7 -12 cm of water. Art. (686-1177 Pa).

The amount of venous return depends on the following components:

circulating blood volume;

intrathoracic pressure values;

body position (with an elevated position of the head end, venous return decreases);

changes in the tone of the veins (capacitance vessels): under the action of sympathomimetics and glucocorticoids, an increase in the tone of the veins occurs; ganglion blockers and adrenolytics reduce venous return;

rhythmic changes in skeletal muscle tone in combination with the work of venous valves;

adequacy of contraction of the atria and appendages of the heart, which provides 20 - 30% of additional filling and stretching of the ventricles.

Among the factors determining the state of venous return, the most important is the BCC. It consists of the volume of formed elements, mainly red blood cells (a relatively constant volume), and the volume of plasma. The latter is inversely proportional to the hematocrit value. Blood volume averages 50 - 80 ml per 1 kg of body weight (5 -7% of weight). The largest part of the blood (up to 75%) is contained in the low-pressure system (venous part of the vascular bed). The arterial section contains about 20% of the blood, and the capillary section contains about 5%. At rest, up to half of the blood volume can be represented by a passive fraction, deposited in organs and included in the blood circulation if necessary (for example, blood loss or muscle work).

For adequate function of the circulatory system, what is important first of all is not the absolute value of the bcc, but the degree to which it corresponds to the capacity of the vascular bed. In weakened patients and in patients with prolonged limitation of mobility, there is always an absolute deficit of BCC, but it is compensated by venous vasoconstriction. Underestimation of this fact often leads to complications during induction of anesthesia, when the use of inducers (for example, barbiturates) relieves vasoconstriction. There is a discrepancy between the BCC and the capacity of the vascular bed, as a result of which venous return and cardiac output decrease.

Modern methods for measuring BCC are based on the principle of diluting indicators, but due to its labor-intensive nature and the need for appropriate equipment, it cannot be recommended for routine clinical use.

Clinical signs of a decrease in blood volume include: pallor of the skin and mucous membranes, decreased blood flow in the peripheral venous bed, tachycardia, arterial hypotension, decreased central venous pressure. None of these signs has independent significance for assessing BCC deficiency, and only their complex use allows for an approximate assessment of it.

Currently, myocardial contractility and peripheral vascular resistance are determined using the concepts preload and afterload .

equivalent to the force that stretches a muscle before it contracts. It is obvious that the degree of stretching of myocardial fibers to diastolic length is determined by the magnitude of venous return. In other words, end-diastolic volume (KDO) equivalent to preload. However, at present there are no routine methods that allow direct measurement of EDV in a clinical setting. A floating (flotation-balloon) catheter inserted into the pulmonary artery makes it possible to measure stall pressure in pulmonary capillaries (DZLK) , which is equal end diastolic pressure nuyu (KDD) in the left ventricle. In most cases, this is true - CVP is equal to EDP in the right ventricle, and PCWP is equal to in the left. However, EDC is equivalent to EDV only when myocardial compliance is normal. Any processes that cause a decrease in extensibility (inflammation, sclerosis, edema, mechanical ventilation with PEEP, etc.) lead to a violation of the correlation between EDP and EDV (to achieve the same EDV value, a larger EDP will be required). Thus, EDC allows one to reliably characterize preload only when ventricular distensibility remains unchanged. In addition, PCWP may not correspond to CD in the left ventricle in aortic insufficiency and in cases of severe pulmonary pathology.

defined as the force that must be overcome by the ventricle to eject the stroke volume of blood. It is equivalent to the transmural stress that occurs in the ventricular wall during systole and includes the following components:

preload;

total peripheral vascular resistance;

pressure in the pleural cavity (negative pressure in the pleural cavity increases afterload, positive pressure decreases).

Thus, afterload is created not only by vascular resistance, it also includes preload, since part of the systolic work of the ventricle is spent on overcoming the latter, as well as a component that is not part of the cardiovascular system.

It is necessary to distinguish contractile ability and contractility of the myocardium . The first is the equivalent of the useful work that the myocardium can perform at optimal values ​​of pre- and afterload, i.e., a potential function. Contractility is an actual function, since it is determined by the work performed by the myocardium at their real values. If pre- and afterload are unchanged, then systolic pressure depends on contractility.

The fundamental law of physiology of the cardiovascular system is for Frank-Starling con: the force of contraction is proportional to the initial length of the myocardial fibers, i.e., the work of the heart depends on the volume of blood in the ventricles at the end of diastole. The first studies, as a result of which these data were obtained, were carried out in 1885 by O. Frank and somewhat later continued by E. Starling. The physiological meaning of the law they formulated (the Frank-Starling law) is that greater filling of the cavities of the heart with blood automatically increases the force of contraction and, therefore, ensures more complete emptying.

As already mentioned, the amount of pressure in the left atrium is determined by the amount of venous support. However, cardiac output increases linearly up to a certain potential, then its increase occurs more gradually. Finally, there comes a point when an increase in end-diastolic pressure does not lead to an increase in cardiac output. The relationship between these quantities approaches linear only in the initial segment of the pressure-volume curve. In general, stroke volume increases until diastolic stretch exceeds 2/3 of maximum stretch. This corresponds to an end-diastolic pressure level of approximately 60 mmHg. Art. If diastolic stretch (filling) exceeds 2/3 of the maximum, then stroke volume stops increasing. In the clinic, such pressure is rarely observed, however, in the case of myocardial pathology, the stroke volume of the heart can decrease even at lower end-diastolic pressure (EDP).

In moderate heart failure, the ability of the ventricle to respond to preload is maintained only when filling pressures exceed normal. This indicates that cardiac output and the level of blood flow at this stage can still be maintained due to the inclusion of compensatory mechanisms (increased venous support), since ventricular activity with moderate failure depends not so much on afterload as on preload. As cardiac function declines further, ventricular activity becomes less dependent on preload. The role of afterload in severe heart failure continues to increase, since vasoconstriction not only reduces cardiac output, but also reduces peripheral blood flow.

Thus, as heart failure progresses, the compensatory function of the increased preload is gradually lost and the pressure of the venous support should not exceed a critical level so as not to cause overdistension of the left ventricle. As ventricular dilatation increases, oxygen consumption also increases proportionally. When diastolic stretch exceeds 2/3 of the maximum, and oxygen demand increases, an “oxygen trap” develops - oxygen consumption is high, but the strength of contractions does not increase. In chronic heart failure, hypertrophied and dilated areas of the myocardium begin to consume up to 27% of all the oxygen the body needs (a sick heart works only on itself).

Physical stress and hypermetabolic states lead to increased contractions of striated muscles, increased heart rate and minute respiratory volume. At the same time, blood flow through the veins increases, central venous pressure, stroke and cardiac output increase.

When the ventricles contract, all the blood is never ejected - a certain amount remains - residualsystolic volume(OSO). Normally, the ejection fraction at rest is about 70%. During normal physical activity, the ejection fraction increases, but the absolute value of TCO remains the same due to an increase in the stroke volume of the heart.

The initial diastolic pressure in the ventricles is determined by the value of TCO. Normally, during physical activity, blood flow and oxygen demand increase, as well as the amount of work performed. Thus, energy expenditure is reasonable, and the efficiency of the heart is not reduced.

With the development of various pathological processes (myocarditis, intoxication, etc.), a primary weakening of myocardial function occurs. It is unable to provide adequate cardiac output, and RCA increases. If the bcc is preserved in the early stages (before the development of systolic dysfunction), this will lead to an increase in diastolic pressure and an increase in the contractile function of the myocardium.

Under unfavorable conditions, the myocardium maintains its stroke volume, but as a result of more pronounced dilatation, the need for oxygen increases. The heart does the same work, but with greater energy costs.

In hypertension, ejection resistance increases. Cardiac minute volume (MCV) either remains unchanged or increases. The contractile function of the myocardium is preserved in the initial stages of the disease, but the heart hypertrophies to overcome the increased resistance to ejection. Then, if hypertrophy progresses, it gives way to dilatation. Energy costs increase, cardiac efficiency decreases. Part of the heart's work is spent on contracting the dilated myocardium, which leads to its exhaustion. Therefore, hypertensive patients often develop left ventricular failure.

In addition, the force of myocardial contraction may increase as a function of presystolic stretch in response to increased rate. Increasing the tone of the sympathetic nervous system also increases the strength of heart contractions. Sympathetic amines, β-adrenostimulants, cardiac glycosides, aminophylline, and Ca 2+ ions have a positive inotropic effect. These substances enhance myocardial contraction regardless of its presystolic filling, but in case of overdose they can cause electrical instability of the myocardium. The contractility of the heart is inhibited by: hypoxia; respiratory and metabolic acidosis (pH< 7,3) и алка­лозом (рН >7.5), necrosis, sclerosis, inflammatory and dystrophic changes in the myocardium; increase or decrease in temperature.

The most important factor in myocardial contractility is the state of coronary blood flow, which depends on diastolic pressure in the aorta, patency of the coronary vessels, blood gas tension, sympathoadrenal activity and is regulated only by the myocardial oxygen demand. The myocardium cannot “borrow oxygen”, and metabolism in the heart cannot occur under conditions of the formation of acidic products and hypoxia. When blood flow stops, metabolism in skeletal muscles continues for another 1.5-2 hours, and in the myocardium it stops after 1-3 minutes. Contractility also depends on the intra- and extracellular content of K +, Na +, Ca 2+, Mg 2+ ions, which provide the strength of muscle contraction and the electrical stability of the myocardium.

The heart is under constant action nervous system and humoral factors. The body is in different conditions of existence. The result of the work of the heart is the pumping of blood into the systemic and pulmonary circulation.

It is estimated by minute blood volume. In a normal state, in 1 minute - 5 liters of blood are pushed out by both ventricles. This way we can evaluate the work of the heart.

Systolic blood volume and heart rate - minute volume of blood.

For comparison between different people - introduced cardiac index- what is the amount of blood per minute per 1 square meter of body.

In order to change the volume value, you need to change these indicators, this happens due to the mechanisms of heart regulation.

Minute blood volume (MBV) = 5 l/min

Cardiac index=IOC/Sm2=2.8-3.6 l/min/m2

IOC=systolic volume*frequency/min

Mechanisms of cardiac regulation

1. Intracardiac (intracardial)
2. Extracardiac (Extracardiac)

To intracardiac mechanisms include the presence of tight junctions between the cells of the working myocardium, the conduction system of the heart coordinates the individual work of the chambers, intracardiac nerve elements, hydrodynamic interaction between the individual chambers.

Extracardiac - nervous and humoral mechanism, which change the work of the heart and adapt the work of the heart to the needs of the body.

Nervous regulation of the heart is carried out by the autonomic nervous system. The heart receives innervation from parasympathetic(wandering) and sympathetic(lateral horns of the spinal cord T1-T5) nerves.

Ganglia of the parasympathetic system lie inside the heart and there the preganglionic fibers switch to postganglionic. Preganglionic nuclei - medulla oblongata.

Sympathetic- are interrupted in the stellate ganglion, where the postganglionic nerves that go to the heart will already be located.

Right vagus nerve- innervates the sinoatrial node, the right atrium,

Left vagus nerve to the atrioventricular node and right atrium

Right sympathetic nerve- to the sinus node, right atrium and ventricle

Left sympathetic nerve- to the atrioventricular nodes and to the left half of the heart.

In the ganglia, acetylcholine acts on N-cholinergic receptors

Sympathetic secrete norepinephrine, which acts on adrenergic receptors (B1)

Parasympathetic- acetylcholine at M-cholino receptors (muscarino)

Effect on heart function.

1. Chronotropic effect (on heart rate)
2. Inotropic (for the strength of heart contractions)
3. Batmotropic effect (on excitability)
4. Dromotropic (for conductivity)

1845 - Weber brothers - discovered the influence of the vagus nerve. They cut the nerve in my neck. When the right vagus nerve is irritated, the frequency of contractions decreases, and could even stop - negative chronotropic effect(suppression of sinus node automation). If the left vagus nerve was irritated, conduction deteriorated. The atrioventricular nerve is responsible for the delay of excitation.

Vagus nerves reduce myocardial excitability and reduce contraction frequency.

Under the influence of the vagus nerve, the diastolic depolarization of p-cells, pacemakers, is slowed down. Potassium output increases. Although the vagus nerve causes cardiac arrest, it cannot be stopped completely. There is a resumption of heart contraction - escaping from the influence of the vagus nerve and the resumption of heart function due to the fact that the automation from the sinus node passes to the atrioventricular node, which returns the heart to work at a frequency 2 times less frequent.

Sympathetic influences- studied by the Zion brothers - 1867. When the sympathetic nerves are irritated, the Zions discovered that the sympathetic nerves give positive chronotropic effect. Pavlov studied further. In 1887 he published his work on the influence of nerves on the functioning of the heart. In his research, he discovered that individual branches, without changing the frequency, increase the strength of contractions - positive inotropic effect. Then the bamotropic and dromotropic effects were discovered.

Positive effects on heart function occurs due to the influence of norepinephrine on beta 1 adrenoceptors, which activate adenylate cyclase, promote the formation of cyclic AMP, and increase the ionic permeability of the membrane. Diastolic depolarization occurs at a faster rate and this causes a more rapid rhythm. Sympathetic nerves increase the breakdown of glycogen and ATP, thereby providing the myocardium with energy resources, and the excitability of the heart increases. The minimum duration of an action potential in the sinus node is set to 120 ms, i.e. theoretically, the heart could give us a number of contractions - 400 per minute, but the atrioventricular node is not capable of conducting more than 220. The ventricles contract maximally at a frequency of 200-220. The role of mediators in the transmission of excitation to the hearts was established by Otto Lewy in 1921. He used 2 isolated frog hearts, and these hearts were fed from the 1st cannula. In one heart, nerve conductors were preserved. When one heart was irritated, he observed what happened in the other. When the vagus nerve is irritated, acetylcholine is released - through the fluid it affects the work of the other heart.

The release of norepinephrine increases the work of the heart. The discovery of this mediator excitation brought Levy the Nobel Prize.

The nerves of the heart are in a state of constant excitement - tone. At rest, the tone of the vagus nerve is especially pronounced. When the vagus nerve is cut, the heart rate increases by 2 times. The vagus nerves constantly inhibit the automation of the sinus node. Normal frequency is 60-100 contractions. Switching off the vagus nerves (transection, cholinergic receptor blockers (atropine)) causes the heart to work faster. The tone of the vagus nerves is determined by the tone of its nuclei. Excitation of the nuclei is maintained reflexively due to impulses that come from the baroreceptors of blood vessels to the medulla oblongata from the aortic arch and carotid sinus. Breathing also affects the tone of the vagus nerves. In connection with breathing - respiratory arrhythmia, when the heart slows down during exhalation.

The tone of the sympathetic nerves of the heart at rest is weakly expressed. If you cut the sympathetic nerves, the frequency of contractions decreases by 6-10 beats per minute. This tone increases with physical activity and increases with various diseases. The tone is well expressed in children and newborns (129-140 beats per minute)

The heart is still susceptible to the action of a humoral factor- hormones (adrenal glands - adrenaline, norepinephrine, thyroid gland - thyroxine and the mediator acetylcholine)

Hormones have a + influence on all 4 properties of the heart. The heart is affected by the electrolyte composition of the plasma and cardiac function changes when the concentration of potassium and calcium changes. Hyperkalemia- increased potassium levels in the blood are a very dangerous condition; this can lead to cardiac arrest in diastole. Hypokalimi I - a less dangerous condition on the cardiogram is a change in the PQ distance, distortion of the T wave. The heart stops in systole. Body temperature also affects the heart - an increase in body temperature by 1 degree - an increase in heart function - by 8-10 beats per minute.

Systolic volume

1. Preload (the degree of stretching of cardiomyocytes before their contraction. The degree of stretching will be determined by the volume of blood that will be in the ventricles.)
2. Contractility (Stretching of cardiomyocytes, where the length of the sarcomere changes. Typically, the thickness is 2 µm. The maximum force of contraction of cardiomyocytes is up to 2.2 µm. This is the optimal ratio between the myosin bridges and actin filaments, when their interaction is maximum. This determines the force of contraction, further stretching up to 2.4 reduces contractility. This adapts the heart to the blood flow, with its increase - the force of contraction of the myocardium can change without changing the amount of blood, due to the hormones adrenaline and norepinephrine, calcium ions, etc. - the force of myocardial contraction increases)
3. Afterload (Afterload is the myocardial tension that must occur in systole for the semilunar valves to open. The amount of afterload is determined by the value of systolic pressure in the aorta and pulmonary trunk)

Laplace's law

Degree of ventricular wall stress = Intragastric pressure * radius / wall thickness. The greater the intraventricular pressure and the larger the radius (the size of the ventricular lumen), the greater the stress of the ventricular wall. An increase in thickness has an inversely proportional effect. T=P*r/W

The amount of blood flow depends not only on minute volume, but it is also determined by the amount of peripheral resistance that occurs in the vessels.

Blood vessels have a powerful influence on blood flow. All blood vessels are lined with endothelium. Next is the elastic framework, and in the muscle cells there are also smooth muscle cells and collagen fibers. The vascular wall obeys Laplace's law. If there is intravascular pressure inside a vessel and the pressure causes stretching in the wall of the vessel, then there is a state of tension in the wall. The radius of the vessels also affects. The voltage will be determined by the product of pressure and radius. In the vessels we can distinguish the basal vascular tone. Vascular tone, which is determined by the degree of contraction.

Basal tone- determined by the degree of stretching

Neurohumoral tone- influence of nervous and humoral factors on vascular tone.

An increased radius puts more stress on the walls of blood vessels than in a can, where the radius is smaller. In order for normal blood flow to occur and adequate blood supply to be ensured, there are vascular regulation mechanisms.

They are represented by 3 groups

1. Local regulation of blood flow in tissue
2. Nervous regulation
3. Humoral regulation

Tissue blood flow provides

Delivery of oxygen to cells

Delivery of nutrients (glucose, amino acids, fatty acids, etc.)

CO2 removal

Removal of H+ protons

Regulation of blood flow- short-term (several seconds or minutes as a result of local changes in tissues) and long-term (occurs over hours, days and even weeks. This regulation is associated with the formation of new vessels in tissues)

The formation of new vessels is associated with an increase in tissue volume and an increase in the metabolic rate in the tissue.

Angeogenesis- formation of blood vessels. This occurs under the influence of growth factors - vascular endothelial growth factor. Fibroblast growth factor and angiogenin

Humoral regulation of blood vessels

1. 1. Vasoactive metabolites

A. Vasodilation is provided by - decrease in pO2, increase - CO2, t, K+ lactic acid, adenosine, histamine

b.vasoconstriction is caused by an increase in serotonin and a decrease in temperature.

2. Influence of the endothelium

Endothelins (1,2,3). - narrowing

Nitric oxide NO - expansion

Formation of nitric oxide (NO)

1. Release of Ach, bradykinin
2. Opening of Ca+ channels in the endothelium
3. Ca+ binding to calmodulin and its activation
4. Enzyme activation (nitric oxide synthetase)
5. Conversion of L fringine to NO

Mechanism of actionNO

NO - activates guanyl cyclase GTP - cGMP - opening of K channels - release of K + - hyperpolarization - decrease in calcium permeability - dilation of smooth muscles and dilation of blood vessels.

Has a cytotoxic effect on bacteria and tumor cells when isolated from leukocytes

Is a mediator of excitation transmission in some neurons of the brain

Mediator of parasympathetic postganglionic fibers for penile vessels

Possibly involved in the mechanisms of memory and thinking

A. Bradikinin

B. Callidin

Kininogen with WWII - bradykinin (with Plasma kallikrein)

Kininogen with YVD - kallidin (with tissue kallikrein)

Kinins are formed during the active activity of the sweat glands, salivary glands and pancreas.

Vascular tone– this is a certain constant tension of the vascular walls, which determines the lumen of the vessel.

Regulation vascular tone is carried out local And systemic nervous and humoral mechanisms.

Thanks to automation some smooth muscle cells of vessel walls, blood vessels, even in the conditions of their denervation, have original(basal )tone , which is characterized self-regulation.

Thus, with an increase in the degree of stretching of smooth muscle cells basal tone increases(especially pronounced in arterioles).

Layers on the basal tone tone, which is provided by nervous and humoral regulation mechanisms.

The main role belongs to the nervous mechanisms that reflexively regulate lumen of blood vessels.

Strengthens basal tone constant tone of the sympathetic centers.

Nervous regulation carried out vasomotors, i.e. nerve fibers that end in muscle vessels (with the exception of exchange capillaries, where there are no muscle cells). IN gas engines refer to autonomic nervous system and are divided into vasoconstrictors(vasoconstriction) and vasodilators(expand).

Most often, sympathetic nerves are vasoconstrictors, since their transection is accompanied by vasodilation.

Sympathetic vasoconstriction is considered a systemic mechanism for regulating the lumen of blood vessels, because it is accompanied by an increase in blood pressure.

The vasoconstrictor effect does not extend to the vessels of the brain, lungs, heart and working muscles.

When the sympathetic nerves are excited, the vessels of these organs and tissues dilate.

TO vasoconstrictors include:

1. Sympathetic adrenergic nerve fibers innervating the vessels of the skin, abdominal organs, parts of skeletal muscles (when interacting norepinephrine with a- adrenergic receptors). Their centers located in all thoracic and three upper lumbar segments of the spinal cord.

2. Parasympathetic cholinergic nerve fibers going to the vessels of the heart. Vasodilator nerves are often part of the parasympathetic nerves. However, vasodilator nerve fibers are also found in the sympathetic nerves, as well as in the dorsal roots of the spinal cord.

TO vasodilators (there are fewer of them than vasoconstrictors) include:

1. Adrenergic sympathetic nerve fibers innervating blood vessels.

Parts of skeletal muscles (when interacting norepinephrine with b- adrenoreceptors);

Hearts (when interacting norepinephrine with b 1 - adrenoreceptors).

2. Cholinergic sympathetic nerve fibers that innervate the vessels of some skeletal muscles.

3. Cholinergic parasympathetic fibers of the vessels of the salivary glands (submandibular, sublingual, parotid), tongue, gonads.

4. Metasympathetic nerve fibers, innervating the vessels of the genital organs.

5. Histaminergic nerve fibers (related to regional or local regulatory mechanisms).

Vasomotor center is a set of structures at various levels of the central nervous system that provide regulation of blood supply.

Humoral regulation vascular tone is carried out by biologically active substances and metabolic products. Some substances dilate, others constrict blood vessels, some have a dual effect.

1. Vasoconstrictors are produced in various cells of the body, but more often in transducer cells (similar to chromaffin cells of the adrenal medulla). The most powerful substance that narrows arteries, arterioles and, to a lesser extent, veins is angiotensin, produced in the liver. However, in blood plasma it is in an inactive state. It is activated by renin (renin-angiotensin system).

As blood pressure decreases, renin production in the kidney increases. Renin by itself does not constrict blood vessels; being a proteolytic enzyme, it breaks down plasma α2-globulin (angiotensinogen) and converts it into a relatively inactive decapeptide (angiotensin I). The latter, under the influence of angiotensinase, an enzyme fixed on the cell membranes of the capillary endothelium, is converted into angiotensin II, which has a strong vasoconstrictor effect, including on the coronary arteries (the mechanism of activation of angiotensin is similar to membrane digestion). Angiotensin also ensures vasoconstriction by activating the sympathetic-adrenal system. Vasoconstrictor effect of angiotensin-

on II, its strength exceeds the influence of nor-adrenaline by more than 50 times. With a significant increase in blood pressure, renin is produced in smaller quantities, blood pressure decreases and returns to normal. Angiotensin does not accumulate in large quantities in the blood plasma, as it is quickly destroyed in the capillaries by angiotensinase. However, in some kidney diseases, as a result of which their blood supply deteriorates, even with normal initial systemic blood pressure, the amount of released renin increases and develops hypertension renal origin.

Vasopressin(ADH is an antidiuretic hormone) also constricts blood vessels, its effects are more pronounced at the level of arterioles. However, vasoconstrictive effects are only well manifested with a significant drop in blood pressure. In this case, a large amount of vasopressin is released from the posterior lobe of the pituitary gland. When exogenous vasopressin is introduced into the body, vasoconstriction is observed, regardless of the initial level of blood pressure. Under normal physiological conditions, its vasoconstrictor effect is not manifested.

Norepinephrine acts mainly on α-adrenergic receptors and constricts blood vessels, as a result of which peripheral resistance increases, but the effects are small, since the endogenous concentration of norepinephrine is low. With exogenous administration of norepinephrine, blood pressure increases, as a result of which reflex bradycardia occurs, cardiac function decreases, which inhibits the pressor effect.

Vasomotor center. Levels of central regulation of vascular tone (spinal, bulbar, hypothalomic cortical). Features of reflex and humoral regulation in the circulatory system in children

Vasomotor center - a set of neurons located at various levels of the central nervous system and regulating vascular tone.
The CNS contains next levels :

spinal;
bulbar;
hypothalamic;
cortical.
2. The role of the spinal cord in the regulation of vascular tone Spinal cord plays a role in the regulation of vascular tone.
Neurons that regulate vascular tone: nuclei of sympathetic and parasympathetic nerves innervating blood vessels. The spinal level of the vasomotor center was discovered in 1870. Ovsyannikov. He cut the central nervous system at various levels and found that in a spinal animal, after removal of the brain, the blood pressure (BP) decreases, but then gradually recovers, although not to the original level, and is maintained at a constant level.
The spinal level of the vasomotor center does not have much independent significance; it transmits impulses from the overlying parts of the vasomotor center.

3. The role of the medulla oblongata in the regulation of vascular tone Medulla oblongata also plays a role in the regulation of vascular tone.
Bulbar section of the vasomotor center opened: Ovsyannikov and Ditegar(1871-1872). In a bulbar animal, the pressure remains almost unchanged, i.e. The main center that regulates vascular tone is located in the medulla oblongata.
Ranson and Alexander. Point irritation of the medulla oblongata revealed that in the bulbar section of the vasomotor center there are pressor and depressor zones. The pressor zone is in the rostral region, the depressor zone is in the caudal region.
Sergievsky, Valdian. Modern views: the bulbar section of the vasomotor center is located at the level of neurons of the reticular formation of the medulla oblongata. The bulbar section of the vasomotor center contains pressor and depressor neurons. They are located diffusely, but in the rostral region there are more pressor neurons, and in the caudal region there are more depressor neurons. The bulbar section of the vasomotor center contains cardioinhibitory neurons. There are more pressor neurons than depressor neurons. That. when the vasomotor center is excited, a vasoconstrictor effect occurs.
There are 2 zones in the bulbar section of the vasomotor center: lateral and medial .
 Lateral zone consists of small neurons that mainly perform an afferent function: they receive impulses from receptors of the heart vessels, internal organs, and exteroceptors. They do not cause a response, but transmit impulses to the neurons of the medial zone.

 Medial zone consists of large neurons that perform an efferent function. They do not have direct contacts with receptors, but receive impulses from the lateral zone and transmit impulses to the spinal vasomotor center.
4. Hypothalamic level of regulation of vascular tone Consider the hypothalamic level of the vasomotor center.
When the anterior groups of hypothalamic nuclei are excited, the parasympathetic nervous system is activated - a decrease in tone. Irritation of the posterior nuclei produces mainly a vasoconstrictor effect.
Features of hypothalamic regulation:

carried out as a component of thermoregulation;

the lumen of blood vessels changes in accordance with changes in the temperature of the environment.
The hypothalamic section of the vasomotor center ensures the use of skin coloring in emotional reactions. The hypothalamic section of the vasomotor center is closely connected with the bulbar and cortical sections of the vasomotor center.
5. Cortical section of the vasomotor center Methods for studying the role of the cortical part of the vasomotor center.
Irritation method: It was discovered that irritated parts of the cerebral cortex, when excited, change vascular tone. The effect depends on the strength and is most pronounced when irritating the anterior central gyrus, frontal and temporal zones of the cerebral cortex.
Conditioned reflex method: It was discovered that the cerebral cortex ensures the development of conditioned reflexes for both dilation and constriction of blood vessels.
Metronome > adrenaline > skin vasoconstriction.
Metronome > saline > cutaneous vasoconstriction.
Conditioned reflexes are developed faster for contraction than for expansion. Due to the cortical part of the vasomotor center, the vascular response adapts to changes in environmental conditions.

In childhood, the functional state of nerve cells is very variable: the level of their excitability changes, and strong or prolonged excitation easily turns into inhibition. This feature of nerve cells explains the instability of the heart rate characteristic of children of early and preschool age. An electrocardiogram, i.e. a graphic recording of heart impulses, using electrical sensors shows that the cycles of heart contractions differ markedly from each other in their duration and height teeth and the duration of the intervals between individual teeth. Reflex changes in the functioning of the heart and blood vessels, in particular the own reflexes of the circulatory system, aimed at maintaining normal blood pressure, are also unstable.

In subsequent years, the stability of both the rhythm of heart contractions and reflex changes in the heart and blood vessels gradually increases. However, for a long time, often up to 15-17 years, increased excitability of the cardiovascular nerve centers persists. This explains the excessive expression of vasomotor and cardiac reflexes in children. They manifest themselves in paleness or, conversely, redness of the skin of the face, a sinking heart or an increase in its contractions.

This regulation is ensured by a complex mechanism, including sensitive (afferent), central And efferent links.

5.2.1. Sensitive link. Vascular receptors - angioceptors- according to their function they are divided into baroreceptors(pressoreceptors) that respond to changes in blood pressure, and chemoreceptors, sensitive to changes in the chemical composition of the blood. Their largest concentrations are in main reflexogenic zones: aortic, sinocarotid, in the vessels of the pulmonary circulation.

An irritant baroreceptors It is not the pressure as such, but the speed and degree of stretching of the vessel wall by pulse or increasing fluctuations in blood pressure.

Chemoreceptors react to changes in the concentration in the blood of O 2, CO 2, H +, and some inorganic and organic substances.

Reflexes that arise from the receptive zones of the cardiovascular system and determine the regulation of relationships within this particular system are called own (systemic) circulatory reflexes. When the strength of stimulation increases, in addition to the cardiovascular system, the response involves breath. It will already be conjugate reflex. The existence of conjugate reflexes makes it possible for the circulatory system to quickly and adequately adapt to the changing conditions of the internal environment of the body.

5.2.2. Central link usually called vasomotor (vasomotor) center. Structures related to the vasomotor center are localized in the spinal cord, medulla oblongata, hypothalamus, and cerebral cortex.

Spinal level of regulation. Nerve cells, the axons of which form vasoconstrictor fibers, are located in the lateral horns of the thoracic and first lumbar segments of the spinal cord and are the nuclei of the sympathetic and parasympathetic system.

Bulbar level of regulation. The vasomotor center of the medulla oblongata is the main center for maintaining vascular tone and reflex regulation of blood pressure.

The vasomotor center is divided into depressor, pressor and cardioinhibitory zones. This division is quite arbitrary, since due to the mutual overlap of the zones it is impossible to determine the boundaries.

Depressor zone helps lower blood pressure by reducing the activity of sympathetic vasoconstrictor fibers, thereby causing vasodilation and a drop in peripheral resistance, as well as by weakening sympathetic stimulation of the heart, i.e., reducing cardiac output.

Pressor zone has the exact opposite effect, increasing blood pressure through an increase in peripheral vascular resistance and cardiac output. The interaction of depressor and pressor structures of the vasomotor center is of a complex synergistic-antagonistic nature.

Cardioinhibitory the action of the third zone is mediated by the fibers of the vagus nerve going to the heart. Its activity leads to a decrease in cardiac output and thereby combines with the activity of the depressor zone in reducing blood pressure.

The state of tonic excitation of the vasomotor center and, accordingly, the level of total blood pressure are regulated by impulses coming from the vascular reflexogenic zones. In addition, this center is part of the reticular formation of the medulla oblongata, from where it also receives numerous collateral excitations from all specifically conducting pathways.

Hypothalamic level of regulation plays an important role in the implementation of adaptive circulatory reactions. The integrative centers of the hypothalamus exert a descending influence on the cardiovascular center of the medulla oblongata, ensuring its control. In the hypothalamus, as well as in the boulevard vasomotor center, there are depressor And pressor zones.

Cortical level of regulationn most thoroughly studied using conditioned reflex methods. Thus, it is relatively easy to develop a vascular reaction to a previously indifferent stimulus, causing sensations of heat, cold, pain, etc.

Certain areas of the cerebral cortex, like the hypothalamus, have a descending influence on the main center of the medulla oblongata. These influences are formed as a result of the comparison of information that entered the higher parts of the nervous system from various receptive zones with the previous experience of the body. They ensure the implementation of the cardiovascular component of emotions, motivations, and behavioral reactions.

5.2.3. Efferent link. Efferent regulation of blood circulation is realized through the smooth muscle elements of the blood vessel wall, which are constantly in a state of moderate tension - vascular tone. There are three mechanisms for regulating vascular tone:

1. autoregulation

2. neural regulation

3. humoral regulation

Autoregulation ensures a change in the tone of smooth muscle cells under the influence of local excitation. Myogenic regulation is associated with changes in the state of vascular smooth muscle cells depending on the degree of their stretching - the Ostroumov-Beilis effect. Smooth muscle cells in the vascular wall respond by contracting to stretch and relaxing to lower pressure in the vessels. Meaning: maintaining a constant level of blood volume entering the organ (the most pronounced mechanism is in the kidneys, liver, lungs, and brain).

Nervous regulation vascular tone is carried out by the autonomic nervous system, which has a vasoconstrictor and vasodilator effect.

Sympathetic nerves are vasoconstrictors(constrict blood vessels) for blood vessels of the skin, mucous membranes, gastrointestinal tract and vasodilators(dilate blood vessels) for the vessels of the brain, lungs, heart and working muscles. Parasympathetic the nervous system has a dilating effect on blood vessels.

Almost all vessels are subject to innervation, with the exception of capillaries. The innervation of veins corresponds to the innervation of arteries, although in general the density of innervation of veins is much less.

Humoral regulation carried out by substances of systemic and local action. Systemic substances include calcium, potassium, sodium ions, hormones:

Calcium ions cause vasoconstriction, potassium ions have an expanding effect.

Biologically active substances and local hormones, such as histamine, serotonin, bradykinin, prostaglandins.

Vasopressin– increases the tone of smooth muscle cells of arterioles, causing vasoconstriction;

Adrenalin it has an effect on the arteries and arterioles of the skin, digestive organs, kidneys and lungs vasoconstrictor effect; on the vessels of skeletal muscles, smooth muscles of the bronchi - expanding, thereby promoting the redistribution of blood in the body. During physical stress and emotional arousal, it helps to increase blood flow through skeletal muscles, brain, and heart. The effect of adrenaline and norepinephrine on the vascular wall is determined by the existence of different types of adrenergic receptors - α and β, which are areas of smooth muscle cells with special chemical sensitivity. Vessels usually contain both types of receptors. The interaction of mediators with the α-adrenergic receptor leads to contraction of the vessel wall, and with the β-receptor - to relaxation.

Atrial natriuretic peptide - m A powerful vasodilator (expands blood vessels, lowering blood pressure). Reduces reabsorption (reabsorption) of sodium and water in the kidneys (reduces the volume of water in the vascular bed). It is released by endocrine cells of the atria when they are overstretched.

Thyroxine– stimulates energy processes and causes constriction of blood vessels;

Aldosterone produced in the adrenal cortex. Aldosterone has an unusually high ability to enhance the reabsorption of sodium in the kidneys, salivary glands, and digestive system, thus changing the sensitivity of the vascular walls to the influence of adrenaline and norepinephrine.

Vasopressin causes narrowing of the arteries and arterioles of the abdominal organs and lungs. However, as under the influence of adrenaline, the vessels of the brain and heart respond to this hormone by dilating, which helps to improve the nutrition of both brain tissue and heart muscle.

Angiotensin II is a product of enzymatic breakdown angiotensinogen or angiotensin I under the influence renina. It has a powerful vasoconstrictor (vasoconstrictor) effect, significantly superior in strength to norepinephrine, but unlike the latter, it does not cause the release of blood from the depot. Renin and angiotensin are renin-angiotensin system.

In nervous and endocrine regulation, hemodynamic mechanisms of short-term action, intermediate and long-term action are distinguished. To the mechanisms short-term actions include circulatory reactions of nervous origin - baroreceptor, chemoreceptor, reflex to CNS ischemia. Their development occurs within a few seconds. Intermediate(in time) mechanisms include changes in transcapillary exchange, relaxation of a tense vessel wall, and the reaction of the renin-angiotensin system. It takes minutes for these mechanisms to turn on, and hours for maximum development. Regulatory Mechanisms long-term actions affect the relationship between intravascular blood volume I capacity of vessels. This is accomplished through transcapillary fluid exchange. This process involves renal fluid volume regulation, vasopressin and aldosterone.

REGIONAL CIRCULATION

Due to the heterogeneity of the structure of different organs, differences in the metabolic processes occurring in them, as well as different functions, it is customary to distinguish between regional (local) blood circulation in individual organs and tissues: coronary, cerebral, pulmonary, etc.

Blood circulation in the heart

In mammals, the myocardium receives blood in two ways coronal(coronary) arteries - right and left, the mouths of which are located in the aortic bulb. The capillary network of the myocardium is very dense: the number of capillaries approaches the number of muscle fibers.

The conditions of blood circulation in the heart vessels differ significantly from the conditions of circulation in the vessels of other organs of the body. Rhythmic fluctuations in pressure in the cavities of the heart and changes in its shape and size during the cardiac cycle have a significant impact on blood flow. So, at the moment of systolic tension of the ventricles, the heart muscle compresses the vessels located in it, so the blood flow weakens, oxygen delivery to tissues is reduced. Immediately after the end of systole, the blood supply to the heart increases. Tachycardia can pose a problem for coronary perfusion because most of the flow occurs during the diastolic period, which becomes shorter as the heart rate increases.

Cerebral circulation

Blood circulation in the brain is more intense than in other organs. The brain requires a constant supply of O 2 and blood flow to the brain is relatively independent of IOC and autonomic nervous activity
systems. Cells of the higher parts of the central nervous system, with insufficient oxygen supply, stop functioning earlier than the cells of other organs. Stopping the blood flow to the cat’s brain for 20 seconds causes the complete disappearance of electrical processes in the cerebral cortex, and stopping the blood flow for 5 minutes leads to irreversible damage to the brain cells.

About 15% of the blood of each cardiac output into the systemic circulation enters the vessels of the brain. With intense mental work, cerebral blood supply increases up to 25%, in children - up to 40%. Cerebral arteries are muscular-type vessels with abundant adrenergic innervation, which allows them to change their lumen over a wide range. The more intense the tissue metabolism, the greater the number of capillaries. In the gray matter, the capillaries are located much denser than in the white matter.

Blood flowing from the brain enters veins that form sinuses in the dura mater of the brain. Unlike other parts of the body, the venous system of the brain does not perform a capacitive function; the capacity of the brain veins does not change, so possible significant changes in venous pressure.

The effectors of cerebral blood flow regulation are intracerebral arteries and pia mater arteries, which are characterized by specific functional features. When total blood pressure changes within certain limits, the intensity of cerebral circulation remains constant. This is accomplished by changing the resistance in the arteries of the brain, which narrow when total blood pressure increases and expand when it decreases. In addition to this autoregulation of blood flow, the protection of the brain from high blood pressure and excessive pulsation occurs mainly due to the structural features of the vascular system in this area. These features consist in the fact that along the vascular bed there are numerous bends (“siphons”). The bends smooth out pressure drops and the pulsating nature of blood flow.

Cerebral blood flow is also determined myogenic autoregulation, in which blood flow is relatively constant over a wide MAP range, from about 60 mmHg to 130 mmHg.

Cerebral blood flow also reacts to changes in local metabolism. Increased neuronal activity and increased O2 consumption cause local vasodilation.

Blood gases also have a strong effect on cerebral blood flow. For example, dizziness during hyperventilation is caused by constriction of cerebral vessels as a result of increased removal of CO 2 from the blood and decreased PaCO 2 . At the same time, the supply of nutrients decreases and the efficiency of brain function is disrupted. On the other hand, an increase in PaCO 2 causes cerebral vasodilation. Variations in PaO2 have little effect, but with severe hypoxia (low PaO2) significant cerebral vasodilation occurs.

Pulmonary circulation

The blood supply to the lungs is carried out by the pulmonary and bronchial vessels. Pulmonary vessels make up the pulmonary circulation and perform mainly gas exchange function between blood and air. Bronchial vessels provide nutrition of lung tissue and belong to the systemic circulation.

A feature of the pulmonary circulation is the relatively short length of its vessels, less (about 10 times compared to the large circle) resistance to blood flow, the thinness of the walls of the arterial vessels and the almost direct contact of the capillaries with the air of the pulmonary alveoli. Due to less resistance, blood pressure in the arteries of the small circle is 5-6 times less than the pressure in the aorta. Red blood cells pass through the lungs in approximately 6 s, staying in the exchange capillaries for 0.7 s.

Blood circulation in the liver

The liver gets simultaneously arterial and venous blood. Arterial blood comes through the hepatic artery, venous blood comes from the portal vein from the digestive tract, pancreas and spleen. The general outflow of blood from the liver into the vena cava is carried out through the hepatic veins. Consequently, venous blood from the digestive tract, pancreas and spleen returns to the heart only after passing additionally through the liver. This feature of the blood supply to the liver, called portal circulation, associated with digestion and barrier function. Blood in the portal system passes through two networks of capillaries. The first network is located in the walls of the digestive organs, pancreas, and spleen; it provides the absorption, excretory and motor functions of these organs. The second network of capillaries is located directly in the liver parenchyma. It ensures its metabolic and excretory functions, preventing intoxication of the body by products formed in the digestive tract.

Research by the Russian surgeon and physiologist N.V. Eck showed that if blood from the portal vein is sent directly to the vena cava, i.e., bypassing the liver, the body will be poisoned with a fatal outcome.

A feature of microcirculation in the liver is the close connection between the branches of the portal vein and the hepatic artery itself with the formation of sinusoidal capillaries, to the membranes of which they are directly adjacent hepatocytes. The large contact surface of blood with hepatocytes and slow blood flow in sinusoidal capillaries create optimal conditions for metabolic and synthetic processes.

Renal circulation

About 750 ml of blood passes through each human kidney within 1 minute, which is 2.5 times the mass of the organ and 20 times the blood supply to many other organs. A total of about 1000 liters of blood passes through the kidneys per day. Consequently, with such a volume of blood supply, the entire amount of blood available in the human body passes through the kidneys within 5-10 minutes.

Blood flows to the kidneys through the renal arteries. They branch out to cerebral And cortical substance, the latter - on glomerular(bringing) and juxtaglomerular. The afferent arterioles of the cortical substance branch into capillaries, which form the vascular glomeruli of the renal corpuscles of the cortical nephrons. The glomerular capillaries collect into the efferent glomerular arterioles. The afferent and efferent arteries differ in diameter by approximately 2 times (the efferent arteries are smaller). As a result of this ratio, unusually high blood pressure occurs in the capillaries of the glomeruli of cortical nephrons - up to 70-90 mm Hg. Art., which serves as the basis for the emergence of the first phase of urine formation, which has the nature of filtering a substance from the blood plasma into the tubular system of the kidneys.

The efferent arterioles, having traveled a short distance, again disintegrate into capillaries. Capillaries intertwine the nephron tubules, forming a peritubular capillary network. This " secondary" capillaries. Unlike “primary” ones, the blood pressure in them is relatively low - 10-12 mm Hg. Art. Such low pressure contributes to the occurrence of the second phase of urine formation, which is in the nature of a process of reabsorption of fluid and the substances dissolved in it from the tubules into the blood. Both arterioles - the afferent and efferent vessels - can change their lumen as a result of contraction or relaxation of the smooth muscle fibers present in their walls.

Unlike general peripheral blood flow, blood flow to the kidneys is not controlled by metabolic factors. Renal blood flow is most strongly influenced by autoregulation and sympathetic tone. In most cases, renal blood flow is relatively constant because myogenic autoregulation operates in the range of 60 mmHg. up to 160 mm Hg. Increased tone of the sympathetic nervous system occurs during exercise or if the baroreceptor reflex stimulates a decrease in blood pressure as a result of renal vasoconstriction.

Blood circulation in the spleen

The spleen is an important hematopoietic and protective organ, varying greatly in volume and weight depending on the amount of blood deposited in it and the activity of hematopoietic processes. The spleen takes part in the elimination of aging or damaged red blood cells and the neutralization of exo- and endogenous antigens that were not retained by the lymph nodes and entered the bloodstream.

The vascular system of the spleen, due to its unique structure, plays a significant role in the function of this organ. The peculiarity of blood circulation in the spleen is due to atypical structure of its capillaries. The terminal branches of the capillaries have brushes ending in blind extensions with holes. Through these holes, the blood passes into the pulp, and from there into the sinuses, which have holes in the walls. Due to this structural feature, the spleen, like a sponge, can deposit large amounts of blood.