Advertising on the portal

What affects vascular tone, how dangerous are changes in pressure in blood vessels? Mechanisms of nervous and humoral regulation of the heart and blood vessels. Reflex and humoral regulation of vascular tone.

In this part we are talking about the nervous and humoral regulation of vascular tone: about the efferent innervation of blood vessels, about a brief description of the vasomotor centers, about the reflex regulation of vascular tone, about the humoral regulation of vascular tone.

Nervous and humoral regulation of vascular tone.

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, we should first of all 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. 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 vascular constriction and blanching of the ear.

The sympathetic nerves, which innervate most of the vessels of the abdominal cavity, approach them as part of the splanchnic nerve. Sympathetic fibers travel to the vessels of the limbs together with motor nerves.

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 (their dilation and expansion) occur due to changes in the number of impulses traveling along the sympathetic nerves. The frequency of these pulses is low - approximately one 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 vasodilating effect only on the vessels of certain 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).

Brief characteristics of vasomotor centers.

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 is called the vasomotor center. 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 the neurons of the pressor center are irritated, vasoconstriction occurs and blood pressure increases, and when the depressor center is irritated, vasodilation occurs and blood pressure decreases. 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, along the fibers of the sympathetic nervous system, impulses go to the muscles of the blood vessels and cause their contraction, as a result of which vasoconstriction occurs.

Reflex regulation of vascular tone.

There are intrinsic cardiovascular reflexes and associated ones.

Conjugate cardiovascular reflexes are divided into two groups: exteroceptive (arising from irritation of receptors lying on the surface of the body) and interoreceptive (arising from irritation of receptors in internal organs).

Any effect on the body that comes from exteroceptors primarily increases the tone of the vasomotor center and causes a pressor reaction. Thus, with mechanical or painful irritation of the skin, strong irritation of the visual and other receptors, a reflex vasoconstriction occurs.

Vascular reactions are associated with the redistribution of blood in the body and the blood supply to working organs.

Particularly important in the redistribution of blood in the body are the reactions that occur when interoreceptors and receptors from working muscles are irritated. Providing working muscles with oxygen and nutrients occurs due to vasodilation and increased blood supply to working muscles. Vasodilation occurs when chemoreceptors are irritated by metabolic products - ATP, lactic, carbonic and other acids, which cause a decrease in tone and dilation of blood vessels. More blood enters the dilated vessels, thereby improving the nutrition of working muscles. But at the same time, redistribution of blood occurs reflexively. Under the influence of efferent impulses from the vasomotor center, vasoconstriction of non-functioning organs occurs. The dilated vessels of working organs turn out to be insensitive to these vasoconstrictor impulses.

Humoral regulation of vascular tone.

Chemicals that affect the lumen of blood vessels are divided into vasoconstrictors and vasodilators.

Adrenaline and norepinephrine have the most powerful vasoconstrictor effects. They cause narrowing of the arteries and arterioles of the skin, lungs and abdominal organs. At the same time, they cause dilation of blood vessels in the heart and brain.

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.

Renin produced in the kidneys has an indirect effect on changes in the lumen of blood vessels and maintaining constant blood pressure. Its formation increases as the amount of sodium in the blood decreases and blood pressure decreases. Interacting with the plasma protein hypertensinogen, it forms the biologically active substance hypertensin, which causes vasoconstriction and an increase in blood pressure.

Vasoconstrictor factors include serotonin, which, by narrowing the damaged vessel, helps reduce bleeding.

Acetylcholine, antihypertensinogen, medulin, bradykinin, prostaglandins, histamine, etc. have a vasodilating effect.

Acetylcholine causes dilation of small arteries and a decrease in blood pressure. Its effect is short-lived, as it is quickly destroyed in the blood.

Antihypertensinogen is constantly in the blood along with hypertensinogen, balancing its effect. Fluctuations in its amount in the blood are aimed at maintaining constant blood pressure.

Medulin is formed in the kidneys, causing vasodilation.

Bradykinin is formed in the tissues of the pancreas and submandibular glands, in the lungs, skin, etc. It reduces the tone of the smooth muscles of arterioles, helping to lower blood pressure.

Histamine is formed in the process of metabolism in skeletal muscles, in the skin, in the walls of the stomach and intestines, etc. Under the influence of histamine, arterioles dilate and the blood supply to the capillaries increases, and therefore a large amount of blood is retained in them. Therefore, blood flow to the heart is reduced, which leads to a drop in blood pressure in the arteries.

Three main mechanisms:

1. Neuromuscular includes afferent and efferent links.

Afferent link The neuromuscular mechanism “collects” information from capillaries, arteries and veins and transmits it to the spinal and (or) bulbar vasomotor centers. The coordinated reaction is realized through the efferent link, which contains monoaminergic and cholinergic axons. Bulbar vasomotor centers provide the necessary blood flow to the main arteries. The entire nervous apparatus is contained in the adventitia.

The functional significance of angioreceptors lies in information about the degree of vascular filling, pressure level, blood flow velocity and the maintenance of cardiovascular homeostasis. Stretch receptors, or mechanoreceptors, are localized mainly in places of high pressure, for example in the aortic reflexogenic zone, which is innervated by the depressor nerves, the carotid body, where the afferent fibers of the sinus nerve end.

Efferent link The vascular system of all arteries, veins and capillaries has an abundance of choline and adrenergic axons. The formation of choline and adrenergic plexuses ends by the age of 25-30, when the plexuses reach their highest level of development and the greatest activity of neurotransmitters is established. In a person under the age of 50, the number of fibers and the level of activity of mediators remain relatively stable, and at an older age both indicators decrease, and individually. All effector fibers are located within the adventitia, and their endings with specific synaptic vesicles are located at a distance of 80-2000 nm from the outer layer of myocytes of the tunica media. Axons have dense vesicles with norepinephrine, light vesicles filled with acetylcholine, brought together at a distance of 20-50 nm.

2. Neuroparacrine regulates the activity of blood vessels through endocrine cells (chromaffinocyte, mast cell), synthesizing peptides (vasopressin, VIP, substance P, etc.), biogenic monoamines and their oxidation products (dopamine, histamine, serotonin, adrenolutin, quinone). Impulses coming from preganglionic cholinergic axons stimulate the level of functional activity of vascular endocrinocytes. Postganglionic monoaminergic axons regulate the synthetic activity of endocrinocytes through the adekylate cyclase system and specific protein kinases. In addition to the nervous system, the inner lining of arteries and veins plays a significant role in the regulation of vascular motility.

3. Endothelium-dependent (intimal) regulation of vascular tone is of decisive importance is the endothelium, which synthesizes factors that prevent blood coagulation (antithrombin III, protein C, plasminogen activator, etc.), activators of the blood coagulation system (thromboplastin, thromboxane A2) and substances with vasomotor activity . Among the vasoactive substances secreted by endothelial cells, prostaglandins, purines, bradykinin, substance P, prostacyclin, serotonin, histamine, etc. are identified. Metabolic products of arachidonic acid and endogenous nitrate - NO take part in the relaxation of blood vessels. Stimuli that cause an endothelial response can be either chemical or mechanical. With the functional integrity of the endothelial layer, biologically active substances (acetylcholine, norepinephrine, prostaglandins, purines) expand the lumen of the vessel, transmitting the effect from the endothelial cell to the myocyte using nitric oxide.

Nervous regulation. The main center for the regulation of cardiac activity is located in the medulla oblongata. Excitation of the sympathetic nerves increases the strength of cardiac contractions (positive inotropic effect), frequency (positive chronotropic effect), excitability (positive bathmotropic effect) and conductivity (positive dromotropic effect) of the heart muscle. Trophic or reinforcing nerve I.P. Pavlova (a branch of the sympathetic nerve) has only a positive inotropic effect. The vagus nerve (parasympathetic) has negative ino-, chrono-, batmo- and dromotropic effects on the heart. The heart is under the tone of the vagus nerve (a constant inhibitory effect on the heart).

Hemodynamic mechanisms of regulation: heterometric regulation (Frank-Starling law) - the more the muscle fibers are stretched during diastole, the greater the blood flow to the heart, the greater the force of heart contractions. Homeometric regulation (does not depend on the initial length of muscle fibers) – Bowditch’s “ladder” (an increase in the frequency of heart contractions with a constant strength of the stimulus leads to an increase in the force of heart contractions), Anrep’s phenomenon (the higher the pressure in the aorta and pulmonary artery, the greater the force of heart contractions ).

Reflex regulation of the heart: intracardiac peripheral reflexes (due to the functioning of the intraorgan nervous system: all parts of the reflex arc are located in the heart), extracardiac mechanisms: reflexes from heart to heart (Bainbridge zone), reflexes from blood vessels to the heart (sinocarotid zone and aortic arch zone ), reflexes from organs to the heart (Goltz and Daninya Aschner reflex).

Humoral regulation of the heart: adrenaline, norepinephrine and dopamine have positive ino-, chrono-, batmo- and dromotropic effects on the heart; acetylcholine - negative foreign, chrono-, batmo- and dromotropic effects; thyroxine – positive chronotropic effect; glucagon – positive ino- and chronotropic effects; corticosteroids and angiotensin – positive inotropic effect. Calcium ions have positive bathmo- and inotropic effects, an overdose causes cardiac arrest in systole; potassium ions (large doses) – negative batmo- and dromotropic effects and cardiac arrest in diastole.

Heart research methods: examination, palpation, percussion, auscultation, determination of systolic and minute blood volumes, electrocardiography, vectorcardiography, phonocardiography, ballistocardiography, echocardiography, etc.

Vascular system. The movement of blood through the vessels is subject to the laws of hemodynamics, which is a branch of hydrodynamics. Functional classification of vessels: shock-absorbing vessels (elastic type vessels); resistive vessels (resistance vessels); sphincter vessels; exchange vessels; capacitive vessels; shunt vessels (arteriovenous anastomoses). Blood circulation parameters: blood pressure; linear blood flow velocity; volumetric blood flow velocity; blood circulation time. Factors determining blood pressure (BP): heart function, resistance and elasticity of the vascular wall, circulating blood mass, blood viscosity, neurohumoral influences. There are systolic, diastolic, pulse and mean arterial pressure. Linear blood flow velocity- the distance that a blood particle travels through vessels of a certain caliber per unit time. Volumetric blood flow velocity- the amount of blood flowing through vessels of a certain caliber per unit of time. Blood circulation rate- the time during which a blood particle passes through the systemic and pulmonary circulation. Arterial pulse- rhythmic oscillations of the artery wall caused by increased pressure during systole. Venous pulse- pulse fluctuations of the wall of a large vein, caused by difficulty in the flow of blood from the veins to the heart during systole of the atria and ventricles.

Microcirculation - processes of blood movement through the smallest blood and lymphatic vessels. Microcirculation includes processes associated with intraorgan blood circulation, which ensures tissue metabolism, redistribution and deposition of blood. In the microcirculation system, there are 2 types of blood flow: slow transcapillary and fast juxtacapillary.

Neurohumoral regulation of vascular tone . Nervous regulation. The main vasomotor center is located in the medulla oblongata. Sympathetic nerves constrict blood vessels; some parasympathetic nerves (glossopharyngeal, lingual, upper laryngeal, pelvic) dilate the vessels of the organ they innervate. The vessels are under constant tone of the sympathetic nerves. Basal tone is due to the vascular wall itself. Additional factors that dilate blood vessels: irritation of the dorsal roots of the spinal cord, axon reflex, irritation of sympathetic cholinergic fibers. Reflex regulation: own reflexes - reflexes from vessels to vessels (sinocarotid and aortic zones) and conjugate reflexes - from organs to vessels. Humoral regulation: vasoconstrictors - adrenaline, norepinephrine, vasopressin, serotonin, renin, endothelin, calcium ions; vasodilators - acetylcholine, histamine, bradykinin, prostaglandins, lactic and pyruvic acids, adenosine, carbon dioxide, nitric oxide, potassium and sodium ions.

Vascular research methods: sphygmography, phlebography, plethysmography, rheography.

The lymphatic system is a drainage system through which tissue fluid flows into the bloodstream (venous system). Lymphatic capillaries are closed. Lymphangion is the area of ​​the lymph vessel between two valves. Lymph nodes are filters that retain microorganisms, tumor cells, and foreign particles; contain T- and B-lymphocytes responsible for immunity; they produce plasma cells that produce antibodies. Functions of the lymphatic system: return proteins, electrolytes and water from the interstitium to the circulatory system; resorptive, barrier, immunobiological, participation in fat metabolism and metabolism of fat-soluble vitamins. Composition of lymph: proteins (albumin, globulins, fibrinogen), lipids, enzymes (lipase and diastase); chlorine and bicarbonates; many lymphocytes, few granulocytes and monocytes.

Lesson 1. Cardiac cycle. Spread of excitation in

heart. Automation. Conduction system of the heart.

Task 1. Cardiac cycle in a frog (Exp. pp. 87-89).

Task 2. Analysis of the cardiac conduction system using the overlay method

ligatures (Stannius ligatures) (Rev. pp. 90-92).

Lesson 2. Properties of the heart muscle. Change in excitability

cardiac muscle in different phases of cardiac

activities. Extrasystole.

Task 1. Reproduction of extrasystole (Ex. p. 98).

Lesson 3. Nervous and humoral regulation of the heart.

Task 1. The influence of irritation of the vago-sympathetic trunk on

activity of the frog's heart. (Exp. pp. 111-113).

Lesson 4. Methods for studying the heart. Electrical phenomena in

heart. Electrocardiography.

Task 1. Registration of an electrocardiogram. (Exp. p. 105).

Task 2. Determination of physical performance (PWC 170 test)

(Exp. p. 436)

Lesson 5. Physiology of blood vessels. Basic laws of hemodynamics.

Task 1. Measuring blood pressure in humans (using the method

Riva-Rochi-Korotkova) (Pr. p. 127).

Task 2. Observation of blood flow in the swimming membrane of the paw

frogs (Ex. p. 136).

Lesson 6. Methods for studying blood flow. Coronary

blood flow

PHYSIOLOGY OF REPEATMENT.

Breath - a complex, cyclically occurring physiological process that ensures gas exchange (O 2 and CO 2) between the environment and the body in accordance with its metabolic needs. The breathing process can be divided into several stages: external respiration (exchange of gases between atmospheric and alveolar air - “pulmonary ventilation”; gas exchange between the blood of the pulmonary capillaries and alveolar air); transport of gases by blood; exchange of gases between blood and body cells; internal or tissue respiration.

External respiration system, includes the lungs and pulmonary circulation (provide arterialization of blood), the chest with respiratory muscles (provide the respiratory act) and the respiratory regulation system (respiratory center and other parts of the central nervous system). Inhale: impulse from the respiratory center - contraction of inspiratory respiratory muscles (diaphragm and external intercostal muscles during quiet inspiration) - increase in chest volume - increase in negative pressure in the pleural cavity - increase in lung volume - decrease in intrapulmonary pressure below atmospheric pressure - entry of air into the lungs. Negative pressure in the pleural cavity caused by elastic traction of the lungs. Elastic traction of the lungs-the force with which the lungs constantly strive to reduce their volume.

Pneumothorax- entry of air into the pleural cavity. Atelectasis- collapse of the alveoli.

Lung volumes and capacities: vital capacity (VC), which includes tidal volume (TI), inspiratory reserve volume (IRV) and expiratory reserve volume (ERV); residual volume (VR); functional residual capacity (FRC=ROvyd+OO); total lung capacity VC+OO); the volume of dead space (air located in the airways and not participating in gas exchange) included in the sediment. Pulmonary ventilation. Minute volume of respiration (MOD = DO x RR). Alveolar ventilation = (DO-volume of dead space) x RR. Gas exchange indicators: oxygen consumption (VO 2), oxygen utilization factor (KIO 2).

Transport of gases by blood. The mechanism of transfer of oxygen from the alveolar air to the blood and carbon dioxide from the blood to the alveolar air is diffusion. Forms of oxygen transfer: oxygen dissolved in plasma; in the form of oxyhemoglobin. Blood oxygen capacity- the maximum amount of oxygen that hemoglobin can bind when it is completely saturated with oxygen. The oxyhemoglobin dissociation curve is the dependence of the binding of oxygen in the blood on its partial pressure. Factors influencing its shifts to the right and left (pCO2, temperature, pH). Forms of carbon dioxide transfer: carbon dioxide dissolved in plasma; in the form of carbhemoglobin; in the form of sodium bicarbonates (in plasma) and potassium (in erythrocytes).

Neurohumoral regulation of breathing. Nervous regulation. Centers: spinal (C3-C5 and T2-T10); bulbar (main), consisting of inspiratory and expiratory sections, possessing automaticity; pons (pneumotaxic). The phrenic nerve and intercostal nerves innervate the respiratory muscles. Reflex regulation - respiratory reflexes begin with various receptors: slowly adapting lung stretch receptors (Hering-Breuer reflex, vagus nerve), irritant rapidly adapting mechanoreceptors (cough, bronchospasm), J-receptors, or " juxtacapillary receptors of the lungs (pulmonary edema), proprioceptors of the respiratory muscles, peripheral (arterial in the carotid sinuses) and central (in the hypothalamus) chemoreceptors. Humoral regulation: Hypercapnia (increased CO2 in the blood), hypoxia (lack of oxygen in tissues) and hydrogen ions (acidosis) stimulate respiration. Hypocapnia (decrease in CO2 in the blood) and hyperoxia (increase in O2 in the alveolar air) depress respiration. Frederick's experience with cross-circulation. Haldane's experiment.

Methods for studying respiratory function: spirometry and spirography, pneumotachography.

Lesson 1. External breathing. Lung volumes and capacities.

Task 1. Spirometry: dry and water spirometers (Ref. page 174).

Task 2. Determination of minute volume of breathing at rest and during

physical activity (Ex. p. 188).

Lesson 2. Gas exchange in the lungs. Transport of gases by blood.

Task 1. Gas analysis of atmospheric, exhaled, alveolar air

using gas analyzers. (Demonstration).

Task 2. Determination of pH, pO 2, pCO 2 in arterialized blood with

using a microanalyzer. (Demonstration).

Lesson 3. Regulation of breathing.

Task 1. Pneumography (Pr. p. 182).

Task 2. Assessing the patency of the tracheobronchial tree using

device "Pneumoscreen-2". (Demonstration).


Related information.


It should be noted that one of important stimulators of nitric oxide synthesis is the mechanical deformation of endothelial cells by the blood flow - the so-called shear deformation of the endothelium.

In addition to nitric oxide, the endothelium produces other vasodilators: prostacyclin (prostaglandin I2), endothelial hyperpolarizing factor, adrenomedulin, C-type natriuretic peptide. The kallikrein-kinin system functions in the endothelium, producing the most powerful peptide dilator bradykinin (Kulikov V.P., Kiselev V.I., Tezov A.A., 1987).

The endothelium also produces vasoconstrictors: endothelins, thromboxane (prostaglandin A2), angiotensin II, prostaglandin H2. Endothelial 1 (ET1) is the most potent of all known vasoconstrictors.

Endothelial factors affect platelet adhesion and aggregation. Prostacyclin is the most important antiplatelet agent, and thromboxane, on the contrary, stimulates platelet adhesion and aggregation.

Violation This balance is referred to as endothelial dysfunction, which plays an important role in the pathogenesis of cardiovascular diseases. The most important laboratory markers of endothelial dysfunction are endothelins and von Willebrand factor.

Humoral-hormonal regulation. It is mainly carried out through the balance of activity of the pressor renin-angiotensin-aldosterone and depressor kallikrein-kinin blood systems. These systems are linked via angiotensin converting enzyme (ACE). ACE converts inactive angiotensin I into angiotensin II, which is a vasoconstrictor and stimulates the production of aldosterone in the adrenal cortex, which is accompanied by water retention in the body and contributes to an increase in blood pressure. At the same time, ACE is the main enzyme for the destruction of bradykinin and thus eliminates its depressor effect. Therefore, ACE inhibitors effectively reduce blood pressure in hypertension, changing the balance of systems towards kinin.

Neurogenic regulation. As already noted, the leading efferent link in the neurogenic control of vascular tone is the sympathetic nervous system. The so-called ischemic reaction of the central nervous system is known. With a significant decrease in systemic blood pressure, ischemia of the vasomotor center and activation of the sympathetic nervous system occurs. The mediator of the latter is norepinephrine, which causes tachycardia (1-receptors) and an increase in vascular tone (1 and 2-receptors).

Afferent link of neurogenic regulation vascular tone is represented by baroreceptors and chemoreceptors located in the aortic arch and carotid sinus.
Baroreceptors respond to the degree and speed of stretching of the vascular wall. Chemoreceptors respond to changes in CO2 concentration in the blood. Sensitive fibers from baroreceptors and chemoreceptors of the aortic arch and carotid sinus pass through the sinocarotid nerve, branches of the glossopharyngeal nerve and depressor nerve.

Neurogenic regulation provides constant (tonic) control over resistive vessels of most vascular areas and emergency reflex regulation, for example, when adopting an orthostatic position. In this and other cases, when the pressure in the carotid sinus and aortic arch drops sharply, the carotid baroreflex is activated, which, through the activation of baroreceptors and the sympathetic nervous system, constricts blood vessels, activates the heart and increases blood pressure. The baroreceptor reflex, on the contrary, is triggered by an increase in blood pressure, which ensures its reduction through inhibition of sympathetic influences and activation of the vagus nerve. The chemoreceptor reflex ensures an increase in blood pressure through the activation of sympathetic influences under conditions of hypoxia, when carbon dioxide accumulates in the blood.

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 was irritated, the frequency of contractions decreased, 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 + effect 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 presented in 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.