Graph of the action potential of typical cardiomyocytes. conduction system of the heart

At rest, the inner surface of the membranes of cardiomyocytes is negatively charged. The resting potential is determined mainly by the transmembrane concentration gradient of K+ ions and in most cardiomyocytes (except for the sinus node and the AV node) it ranges from minus 80 to minus 90 mV. When excited, cations enter the cardiomyocytes, and their temporary depolarization occurs - the action potential.

The ionic mechanisms of the action potential in working cardiomyocytes and in the cells of the sinus node and the AV node are different, therefore the shape of the action potential also differs (Fig. 230.1).

The action potential of the cardiomyocytes of the His-Purkinje system and the working myocardium of the ventricles has five phases (Fig. 230.2). The phase of rapid depolarization (phase 0) is due to the entry of Na+ ions through the so-called fast sodium channels. Then, after a brief phase of early rapid repolarization (phase 1), a phase of slow depolarization, or a plateau, occurs (phase 2). It is due to the simultaneous entry of Ca2+ ions through slow calcium channels and the release of K+ ions. The phase of late rapid repolarization (phase 3) is due to the predominant release of K + ions. Finally, phase 4 is the resting potential.

Bradyarrhythmias can be caused either by a decrease in the frequency of action potentials, or by a violation of their conduction.

The ability of some heart cells to spontaneously generate action potentials is called automatism. This ability is possessed by the cells of the sinus node, the atrial conduction system, the AV node and the His-Purkinje system. Automaticity is due to the fact that after the end of the action potential (that is, in phase 4), instead of the rest potential, the so-called spontaneous (slow) diastolic depolarization is observed. Its cause is the entry of Na+ and Ca2+ ions. When, as a result of spontaneous diastolic depolarization, the membrane potential reaches the threshold, an action potential occurs.

Conductivity, that is, the speed and reliability of excitation, depends, in particular, on the characteristics of the action potential itself: the lower its steepness and amplitude (in phase 0), the lower the speed and reliability of conduction.

In many diseases and under the influence of a number of drugs, the rate of depolarization in phase 0 decreases. In addition, conductivity also depends on the passive properties of cardiomyocyte membranes (intracellular and intercellular resistance). Thus, the speed of excitation conduction in the longitudinal direction (that is, along the myocardial fibers) is higher than in the transverse direction (anisotropic conduction).

During the action potential, the excitability of cardiomyocytes is sharply reduced - up to complete non-excitability. This property is called refractoriness. During the period of absolute refractoriness, no stimulus is able to excite the cell. During the period of relative refractoriness, excitation occurs, but only in response to suprathreshold stimuli; the rate of excitation is reduced. The period of relative refractoriness continues until the complete restoration of excitability. There is also an effective refractory period, during which excitation can occur, but is not carried out outside the cell.

In the cardiomyocytes of the His-Purkinje system and the ventricles, excitability is restored simultaneously with the end of the action potential. On the contrary, in the AV node, excitability is restored with a significant delay. Heart: connection between excitation and contraction.

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Propagation of the potential along the axon. , CC BY-SA 3.0, Link

Cardiomyocytes have a negative and constant electrical potential, which contains about -85 mV. These cells are not capable of self-excitation, they are excited by an electrical current floating from a neighboring excited cardiomyocyte through close connections. If the voltage of this flow is large enough to depolarize the cell membrane to -65 mV ( threshold potential), then the following happens:

1. the permeability of ion channels in the cell membrane changes;
2. depolarizing sodium and calcium ions penetrate the membrane, and then repolarizing potassium currents. What is accompanied by a short-term and instant increase in cellular potential ().

Repolarization is a consequence of the inactivation of sodium and calcium channels and the opening of potassium channels. The proportions of ion flows through all these channels indicate the length of the action potential, the refractive period (the period of non-excitability of the cell during the action potential) and the QT segment on the ECG.

The action potential of cardiomyocytes acts as a trigger for contraction, triggers a number of cellular processes called electromechanical interface, which consists of:

1. increase in intracellular concentration of calcium ions (Ca 2+);
2. activation of contractile proteins;
3. contraction of the cardiomyocyte;
4. release of Ca 2+ from the cytoplasm;
5. relaxation of the cardiomyocyte.

Each action potential of cardiomyocytes is accompanied by the opening (activation) of type L calcium ion channels and, according to the intercellular electrochemical gradient, the movement of Ca 2+ to a narrow submembrane space, which is located between the cell membrane and the membranes of the terminal vesicles of the sarcoplasmic reticulum, which is the storage of calcium in the cell.

The role of calcium in myocardial contraction

An increase in the concentration of Ca 2+ in the submembrane space is the cause of the following: the opening of calcium channels in the membrane of the sarcoplasmic reticulum (the so-called ryanodine receptors), the release of Ca 2+ deposited there from the reticulum and a rapid increase in its concentration in the cytoplasm. It comes to the binding of calcium to its protein receptor - troponin C in the contractile apparatus, which makes it possible for the contractile proteins to interact with each other (actin and myosin) and to contract the cell in proportion to the number of calcium-troponin complexes.

Calcium ATPase again captures a certain amount of Ca 2+ ions to the sarcoplasmic reticulum, where they are deposited until the next action potential of cardiomyocytes initiating the next one. The rest of the calcium is removed from the cell by the membrane ion transporter, which carries one calcium ion out of the cell and in return brings 3 sodium ions into the cell (Na/Ca exchanger). An important role in the removal of calcium from the cell is also played by calcium ATPase in the cell membrane.

Myocardial cells are excitable, but not automatic. During diastole resting membrane potential of these cells is stable, and its value is higher (80-90 mV) than in the cells of pacemakers. The action potential in these cells arises under the influence of excitation of pacemaker cells, which reaches cardiomyocytes, causing depolarization of their membranes.

Cell action potential the working myocardium consists of a phase of rapid depolarization, initial rapid repolarization, turning into a phase of slow repolarization (plateau phase), and a phase of rapid final repolarization (Fig. 9.8). The rapid depolarization phase is created by a sharp increase in the permeability of the membrane to sodium ions, which leads to a rapid incoming sodium current. The latter, however, upon reaching the membrane potential of 30-40 mV, is inactivated and subsequently, up to potential inversion (about +30 mV) and in the “plateau” phase, calcium ion currents play a leading role. Depolarization of the membrane causes the activation of calcium channels, resulting in an additional depolarizing incoming calcium current.

terminal repolarization in myocardial cells is due to a gradual decrease in membrane permeability to calcium and an increase in permeability to potassium. As a result, the incoming calcium current decreases and the outgoing potassium current increases, which ensures a rapid restoration of the resting membrane potential. The duration of the action potential of cardiomyocytes is 300-400 ms, which corresponds to the duration of myocardial contraction (Fig. 9.9).

At rest, the inner surface of the membranes of cardiomyocytes is negatively charged. The appearance of the membrane potential of cardiomyocytes is due to selective permeability of their membrane for potassium ions. Its value in contractile cardiomyocytes is 80-90 mV They have the following phases:

1. Depolarization phase(by opening the sodium and calcium channels of the membrane, through which these ions enter the cytoplasm);

2. Rapid initial repolarization phase(fast inactivation of sodium and slow calcium channels. Potassium channels are activated at the same time)

3. Phase of delayed repolarization

4. Rapid terminal repolarization phase

The duration of AP of cardiomyocytes is 200-400 ms.

At the action potential of cardiomyocytes of the His-Purkinje system and the working myocardium of the ventricles, five phases:

*Fast depolarization phase ( phase 0) is due to the entry of Na+ ions through the so-called fast sodium channels.

*Then, after a brief phase of early rapid repolarization ( phase 1),

*the phase of slow depolarization begins, or plateau ( phase 2). It is due to the simultaneous entry of Ca2+ ions through slow calcium channels and the release of K+ ions.

*Phase of late rapid repolarization ( phase 3) is due to the predominant yield of K+ ions.

*Finally, phase 4 is the resting potential.

The ability of certain cells in the heart to spontaneously form action potentials is called automatism. This ability is possessed by the cells of the sinus node, the atrial conduction system, the AV node and the His-Purkinje system.

Potential dependent ion channels: sodium and calcium channels(consists of the main a-subunits With 4 transmembrane subunits, each consists of 624 spirals, twisted together and form one functioning pore of each calcium channel) and some of the potassium channels (simply arranged).

Activation at the molecular level is a change in the charge of the 4th transmembrane segment - the polarization sensor, of each of the 4 subunits of the sodium or calcium channel. a-Subunit enhances the current of calcium through the pores. Channels range from fully closed to fully open

Action potentials (AP), registered in different parts of the heart using intracellular microelectrodes,

Refractory period- the period of time after the appearance of an action potential on the excitable membrane, during which the excitability of the membrane decreases, and then gradually recovers to its original level.

The refractory period is due to the peculiarities of the behavior of voltage-dependent sodium and voltage-dependent potassium channels of the excitable membrane.

During PD, voltage-gated sodium (Na+) and potassium (K+) channels switch from state to state. At Na+ ground state channels three - closed, open and inactivated. At K+ channels two main states closed and open.

During membrane depolarization during AP, Na+ channels after the open state temporarily become inactivated, while K+ channels open and remain open for some time after the end of AP, creating an outgoing K+ current that brings the membrane potential to the initial level.

As a result of inactivation of Na+ channels, an absolute refractory period occurs. Later, when some of the Na+ channels have already left the inactivated state, PD may arise.

25 . Postsynaptic potential (PSP)- this is a temporary change in the potential of the postsynaptic membrane in response to a signal received from the presynaptic neuron.

Distinguish:

* excitatory postsynaptic potential (EPSP), which provides depolarization of the postsynaptic membrane, and

* inhibitory postsynaptic potential (IPSP), which provides hyperpolarization of the postsynaptic membrane.

Conventionally, the probability of triggering an action potential can be described as resting potential + sum of all excitatory postsynaptic potentials - sum of all inhibitory postsynaptic potentials > threshold for triggering an action potential.

Individual PSPs are usually small in amplitude and do not cause action potentials in the postsynaptic cell; however, unlike action potentials, they are gradual and can be summed up. There are two summation options:

*temporary- combining the signals that came through one channel (when a new impulse arrives before the previous one fades);

*spatial- superposition of EPSPs of adjacent synapses;

The mechanism of occurrence of PSP. When an action potential arrives at the presynaptic terminal of a neuron, the presynaptic membrane is depolarized and voltage-gated calcium channels are activated. Calcium begins to enter the presynaptic ending and causes exocytosis of vesicles filled with a neurotransmitter. The neurotransmitter is released into the synaptic cleft and diffuses to the postsynaptic membrane. On the surface of the postsynaptic membrane, the neurotransmitter binds to specific protein receptors (ligand-gated ion channels) and causes them to open.

26. Reduction- this is a change in the mechanical state of the myofibrillar apparatus of muscle fibers under the influence of nerve impulses. In 1939, Engelhardt and Lyubimova established that myosin has the properties of the enzyme adenosine triphosphatase, which breaks down ATP. It was soon established that when actin interacts with myosin, a complex is formed - actomyosin, the enzymatic activity of which is almost 10 times higher than the activity. During this period, the development of the modern theory of muscle contraction began, which was called the theory of sliding threads. According to this theory of "sliding", contraction is based on the interaction between actin and myosin filaments of myofibrils due to the formation of transverse bridges between them.

During gliding, the actin and myosin filaments themselves do not shorten, but the length of the sarcomere (the basic contractile unit of striated muscle, which is a complex of several proteins consisting of three different fiber systems) changes. In a relaxed, and even more so, stretched muscle, active filaments are located farther from the center of the sarcomere, and the length of the sarcomere is greater. During isotonic muscle contraction, the actin filaments slide towards the center of the sarcomere along the myosin filaments. The actin filaments are attached to the Z-membrane, pulling it along, and the sarcomere shortens. The total shortening of all sarcomeres causes shortening of the myofibrils, and the muscle contracts.

The following model of actin filament glide is currently accepted.

The excitation impulse along the motor neuron reaches the neuromuscular synapse - the end plate, where acetylcholine is released, which interacts with the postsynaptic membrane, and an action potential arises in the muscle fiber, i.e. muscle fibers are stimulated.

When Ca ++ ions bind to troponin (whose spherical molecules "sit" on actin chains), the latter is deformed, pushing tropomyosin into the grooves between the two actin chains. In this case, the interaction of actin with myosin heads becomes possible and a contraction force arises. The myosin heads make "stroke" movements and move the actin filament towards the center of the sarcomere.

Myosin filaments have many heads; they pull the actin filament with a combined, total force. With the same rowing movement of the heads, the sarcomere is shortened by about 1% of its length (and with isotonic contraction, the muscle sarcomere can be shortened by 50% of the length in tenths of a second), therefore, the transverse bridges should make about 50 "stroke" movements for the same period of time.

The cumulative shortening of successively located myofibril sarcomeres leads to a marked contraction of the muscle. At the same time, ATP hydrolysis occurs. After the end of the peak of the action potential, the calcium pump (Ca - dependent ATP-ase) of the membrane of the sarcoplasmic reticulum is activated. Due to the energy released during the breakdown of ATP, the calcium pump pumps Ca ++ ions back into the cisterns of the sarcoplasmic reticulum, where Ca ++ is bound by protein calsequestrin.

The concentration of Ca ++ ions in the muscle cytoplasm decreases to 10 - 8 m, and in the sarcoplasmic reticulum it rises to 10 -3 m.

A decrease in the level of Ca ++ in the sarcoplasm inhibits the ATP-ase activity of actomyosin; in this case, the cross bridges of myosin are disconnected from actin. Relaxation occurs, muscle lengthening as a result of passive movement (without energy expenditure).

Thus, muscle contraction and relaxation is a series of processes that unfold in the following sequence: a nerve impulse - the release of acetylcholine by the presynaptic membrane of the neuromuscular synapse - the interaction of acetylcholine with the postsynaptic membrane of the synapse - the occurrence of an action potential - electromechanical coupling (conduction of excitation through T-tubules, release of Ca ++ and its effect on the troponin-tropomyosin-actin system) - the formation of cross bridges and the "sliding" of actin filaments along myosin filaments - a decrease in the concentration of Ca ++ ions due to the operation of the calcium pump - a spatial change in the proteins of the contractile system - relaxation of myofibrils.

After death, the muscles remain tense, the so-called rigor mortis, since the cross-links between the actin and myosin filaments cannot be broken due to the lack of ATP energy and the inability of the calcium pump to work.

27. Fur-m of carrying out excitation along unmyelinated nerve fibers. At rest, the entire inner surface of the nerve fiber membrane carries a negative charge, and the outer side of the membrane is positive. Electric current between the inner and outer sides of the membrane does not flow, since the lipid layer of the membrane has a high electrical resistance. During the development of the action potential in the excited region of the membrane, a charge reversion occurs. At the border of the excited and unexcited area, an electric current begins to flow. An electric current irritates the nearest section of the membrane and brings it into a state of excitation, while the previously excited sections return to a state of rest. Thus, a wave of excitation covers all new sections of the nerve fiber membrane.

AT myelinated nerve fiber sections of the membrane, covered with a myelin sheath, are non-excitable; excitation can occur only in areas of the membrane located in the region of Ranvier's intercepts. With the development of an action potential in one of the nodes of Ranvier, the membrane charge is reversed. An electric current arises between the electronegative and electropositive sections of the membrane, which irritates neighboring sections of the membrane. However, only a section of the membrane in the region of the next node of Ranvier can go into a state of excitation. Thus, excitation spreads across the membrane in a jump-like manner from one node of Ranvier to another.

28. An action potential is a wave of excitation that moves along the membrane of a living cell in the process of transmitting a nerve signal. In essence, it represents an electrical discharge - a quick short-term change in potential on a small section of the membrane of an excitable cell (neuron, muscle fiber or glandular cell), as a result of which the outer surface of this section becomes negatively charged with respect to neighboring sections of the membrane, while its inner surface becomes positively charged with respect to neighboring regions of the membrane. The action potential is the physical basis of a nerve or muscle impulse that plays a signal (regulatory) role.

Action potentials can differ in their parameters depending on the type of cell and even on different parts of the membrane of the same cell. The most characteristic example of differences is the action potential of the heart muscle and the action potential of most neurons. However, the following phenomena underlie any action potential:

The membrane of a living cell is polarized - its inner surface is negatively charged with respect to the outer one due to the fact that in the solution near its outer surface there are more positively charged particles (cations), and near the inner surface there are more negatively charged particles (anions). ).

The membrane has selective permeability - its permeability for various particles (atoms or molecules) depends on their size, electric charge and chemical properties.

The membrane of an excitable cell is able to quickly change its permeability to a certain type of cations, causing a positive charge to pass from the outside to the inside.

The first two properties are characteristic of all living cells. The third is a feature of the cells of excitable tissues and the reason why their membranes are able to generate and conduct action potentials.

Action potential phases

prespike- the process of slow depolarization of the membrane to a critical level of depolarization (local excitation, local response).

Peak Potential, or a spike consisting of an ascending portion (membrane depolarization) and a descending portion (membrane repolarization).

Negative trace potential- from the critical level of depolarization to the initial level of membrane polarization (trace depolarization).

Positive trace potential- an increase in the membrane potential and its gradual return to its original value (trace hyperpolarization).

Ion channels are pore-forming proteins (single or whole complexes) that maintain the potential difference that exists between the outer and inner sides of the cell membrane of all living cells. They are transport proteins. With their help, ions move according to their electrochemical gradients through the membrane. Such complexes are a set of identical or homologous proteins densely packed in the lipid bilayer of the membrane around the water pore. Channels are located in the plasmalemma and some of the inner membranes of the cell.

Na + (sodium), K + (potassium), Cl - (chlorine) and Ca ++ (calcium) ions pass through the ion channels. Due to the opening and closing of ion channels, the concentration of ions on different sides of the membrane changes and the membrane potential shifts.

Channel proteins consist of subunits that form a structure with a complex spatial configuration, in which, in addition to the pore, there are usually molecular systems of opening, closing, selectivity, inactivation, reception, and regulation. Ion channels may have several sites (sites) for binding to the controlling in-you.

29. Myogenic regulation. The study of the dependence of the force of contractions of the heart on the stretching of its chambers showed that the force of each heart contraction depends on the magnitude of the venous inflow and is determined by the final diastolic length of the myocardial fibers. As a result, a rule was formulated that entered physiology as Starling's law: "The force of contraction of the ventricles of the heart, measured in any way, is a function of the length of the muscle fibers before contraction."

Inotropic effects on the heart, due to the Frank-Starling effect, can manifest themselves under various physiological conditions. They play a leading role in increasing cardiac activity during increased muscular work, when contracting skeletal muscles cause periodic compression of the veins of the extremities, which leads to an increase in venous inflow due to the mobilization of the reserve of blood deposited in them. Negative inotropic influences by this mechanism play a significant role in changes in blood circulation during the transition to a vertical position (orthostatic test). These mechanisms are of great importance for coordinating changes in cardiac output and blood flow through the veins of the small circle, which prevents the risk of developing pulmonary edema. Heterometric regulation of the heart can provide compensation for circulatory insufficiency in its defects.

The term "homeometric regulation" refers to myogenic mechanisms, for the implementation of which the degree of end-diastolic stretching of myocardial fibers does not matter. Among them, the most important is the dependence of the force of contraction of the heart on the pressure in the aorta (the Anrep effect). This effect is that an increase in aortic pressure initially causes a decrease in the systolic volume of the heart and an increase in the residual end-diastolic blood volume, followed by an increase in the force of contractions of the heart, and cardiac output stabilizes at a new level of force of contractions.

Neurogenic regulation- one of the mechanisms of a complex system of regulation of blood circulation in the human body. Neurogenic regulation is short-term and allows the body to quickly and effectively adapt to abrupt changes in hemodynamics associated with changes in blood volume, cardiac output, or peripheral resistance.

Humoral effects on the heart. Almost all biologically active substances contained in the blood plasma have a direct or indirect effect on the heart. These are the catecholamines secreted by the medulla of the adrenal glands - adrenaline, norepinephrine and dopamine. The action of these hormones is mediated by beta-adrenergic receptors of cardiomyocytes, which determines the final result of their effects on the myocardium. It is similar to sympathetic stimulation and consists in the activation of the enzyme adenylate cyclase and increased synthesis of cyclic AMP (3,5-cyclic adenosine monophosphate), followed by activation of phosphorylase and an increase in the level of energy metabolism.

The action of other hormones on the myocardium is nonspecific. The inotropic effect of glucagon is known. The hormones of the adrenal cortex (corticosteroids) and angiotensin also have a positive inotropic effect on the heart. Iodine-containing thyroid hormones increase the heart rate.

The heart is also sensitive to the ionic composition of the flowing blood. Calcium cations increase the excitability of myocardial cells.

Innervation of the heart. The heart is a richly innervated organ. A large number of receptors are located in the walls of the cardiac chambers and in the epicardium. The most important among the sensitive formations of the heart are two populations of mechanoreceptors, concentrated mainly in the atria and left ventricle: A-receptors respond to changes in the tension of the heart wall, and B-receptors are excited when it is passively stretched. Afferent fibers associated with these receptors are part of the vagus nerves. Free sensory nerve endings, located directly under the endocardium, are the terminals of afferent fibers that pass through the sympathetic nerves. It is believed that these structures are involved in the development of pain syndrome with segmental irradiation, which is characteristic of attacks of coronary heart disease, including myocardial infarction.

The efferent innervation of the heart is carried out with the participation of both parts of the autonomic nervous system.

The bodies of sympathetic preganglionic neurons involved in the innervation of the heart are located in the gray in the lateral horns of the three upper thoracic segments of the spinal cord.

The derivatives of the vagus nerve, passing through the cardiac nerves, are parasympathetic preganglionic fibers. From them, excitation is transmitted to intramural neurons and then - mainly to the elements of the conduction system.

30. Numerous experiments have shown that various products of metabolic reactions can act as irritants not only directly on cell membranes, but also on nerve endings - chemoreceptors, causing certain physiological and biochemical changes in a reflex way. In addition, physiologically active substances, being carried by the blood stream throughout the body, only in certain places, in the resulting organs or target cells, cause purposeful specific reactions when interacting with effectors or the corresponding receptor formations.

So, many transmitters of nerve influence - mediators, having fulfilled their main role and avoiding enzymatic inactivation or reuptake by nerve endings, enter the bloodstream, performing a distant (non-transmitter) action. Penetrating through histohematic barriers, they enter organs and tissues and regulate their vitality. The condition of the nervous system itself depends not only on information from the external and internal environment, but also on the blood supply and on the various ingredients of the internal environment.

In this case, there is a close relationship and interdependence of nervous and humoral processes. So, the neurosecretory cells of the hypothalamic nuclei are the site of the transformation of nerve stimuli into humoral ones, and humoral ones into nervous ones. In addition to various mediators, numerous peptides and other active compounds are synthesized in the brain, which are involved in the regulation of the activity of the brain and spinal cord, and when they enter the bloodstream, the entire org-ma. Thus, and the brain can also be called an endocrine gland.

The physiological activity of liquid org-ma media is largely due to the ratio of electrolytes and microelements, the state of synthesizing and degrading enzyme systems, the presence of activators and inhibitors, the formation and breakdown of complex protein-polysaccharide complexes, the binding and release of substrates of unbound forms, etc.

An important role in the neurohumoral regulation of functions is played by hormones, as well as a variety of specific and nonspecific products of interstitial metabolism, united under the general name metabolites. These include tissue hormones, hypothalamic neurohormones, prostaglandins, and broad-spectrum oligopeptides.

Increasing importance in the integration of neurons in the centers, in the creation of their operational constellations, in the coordination relations between them, is attached to the direct humoral background, the microsphere in the brain, created, in particular, by the secretion of the neurons themselves. This circumstance once again testifies to the unity of the nervous and humoral mechanisms.

What are the advantages obes-t method of regulation f-th, carried out with the predominant participation of the nervous apparatus? In contrast to the humoral connection, the nervous connection, firstly, has an exact direction to a specific organ and even a group of cells, and, secondly, through the nerve conductors, the connection is carried out at a much higher speed, hundreds of times higher than the rate of distribution of physiologically active substances. Along with the cable control method according to the "subscriber-response" principle, as at a telephone exchange, the central apparatus of the nervous system with predominant integrative intermediate neurons provides a probabilistic control principle, flexibly adapted to a continuously changing environment and providing deterministic executive reactions.

31. The exchange of in-in and energy underlies all manifestations of life and represents the co-th processes of transformation in-in and energy in a living organism and the exchange of in-you and energy between the organism and the environment. To maintain vitality in the process of exchanging in-in and energy, the plastic and energy needs of the organism are provided. Plastic needs are met at the expense of the in-in used to build biological structures, and energy - by converting the chemical energy of the nutrients entering the org-m into the energy of high-energy and reduced compounds. Their energy is used by the organism to synthesize proteins, nucleic acids, lipids, as well as components of cell membranes and cell organelles, to perform cell activities associated with the use of chemical, electrical and mechanical energy. The exchange of in-in and energy (metabolism) in the human org-me is an owl of interrelated, but multidirectional processes: anabolism (assimilation) and catabolism (dissimilation). Anabolism- this is the cov-th of the processes of biosynthesis of organic substances, components of the cell and other structures of organs and tissues. catabolism- these are the processes of splitting complex molecules, components of cells, organs and tissues to simple substances and to the final products of metabolism. In the vast majority of animals, body temperature changes with changes in ambient temperature. Such animals, unable to regulate their body temperature, are called poikilothermic animals. Only an insignificant minority of animal species in the course of their phylogeny acquired the ability to actively regulate body temperature; such animals with a relatively constant body temperature are called homoiothermic. In mammals, the body temperature is usually 36-37°C, in birds it rises to about 40°C. The influence of sharp fluctuations in ambient temperature on org-we reduce special adaptive complexes of signs.

There are two fundamentally different types of temperature adaptations: passive and active. The first type is characteristic of ectothermic (poikilothermic, cold-blooded) organisms (all taxa of the organic world, except for birds and mammals). Their activity depends on the ambient temperature: insects, lizards and many other animals become lethargic and inactive in cool weather. At the same time, many animal species have the ability to choose a place with optimal conditions for temperature, humidity and insolation (when there is a shortage of heat, lizards bask on rock slabs illuminated by the sun, and when there is an excess of it, they hide under stones and burrow into the sand). Ectothermic organisms have special adaptations for experiencing cold - the accumulation of “biological antifreezes” in cells that prevent water from freezing and the formation of ice crystals in cells and tissues. For example, in cold-water fish such antifreezes are glycoproteins, in plants - sugar. Endothermic (homeothermic, warm-blooded) organisms (birds and mammals) are provided with heat due to their own heat production and are able to actively regulate heat production and its consumption. At the same time, their body temperature changes insignificantly, its fluctuations do not exceed 2–4°C even in the most severe frosts.

The main adaptations are chemical thermoregulation due to heat release (for example, aspiration) and physical thermoregulation due to heat-insulating structures (fat, feathers, hair, etc.). Endothermic, as well as ectothermic animals, use the cooling mechanisms of evaporation of moisture from the mucous membranes of the oral cavity and upper respiratory tract to lower body temperature. Fever is a typical thermoregulatory protective and adaptive response of the body to the effects of pyrogenic substances, expressed as a temporary restructuring of heat transfer to maintain a higher than normal heat content and body temperature.

It is assumed that there are three types of thermoregulatory neurons in the hypothalamus: 1) afferent neurons that receive signals from peripheral and central thermoreceptors; 2) intercalary, or interneurons; 3) efferent neurons, whose axons control the activity of effectors of the thermoregulation system.

32. Exchange in-in between the org-mom and the external environment - the main and inalienable property of life. The data of modern biochemistry show with complete certainty that without exception, all organs and tissues of a person (even such as bones and teeth) are in a state of continuous exchange of substances, constant chemical interaction with other organs and tissues, as well as with the surrounding org. external environment. It has also been established that an intensive exchange of v-v occurs not only in the cytoplasm of the cell, but also in all parts of its nuclear apparatus, in particular in the chromosomes.

The basis of the exchange in-in are the processes of catabolism and anabolism.

catabolism- cos of the enzymatic reactions of the breakdown of complex organic substances, including food ones, occurring in a living organism. In the process of catabolism, also called dissimilation, the energy contained in the chemical bonds of large organic molecules is released and stored in the form of energy-rich ATP bonds. Catabolic processes include cellular respiration, glycolysis, and fermentation. The main end products of catabolism are water, carbon dioxide, ammonia, urea, lactic acid, which are excreted from the body through the skin, lungs and kidneys.

Allocate two types of action potential(PD): quick(atrial and ventricular myocytes (0.3-1 m/s), Purkinje fibers (1-4)) and slow(SA-pacemaker of the 1st order (0.02), AV-pacemaker of the 2nd order (0.1)).

Main types of ion channels in the heart:

1) Fast sodium channels(we block with tetrodotoxin) - cells of the atrial myocardium, working ventricular myocardium, Purkinje fibers, atrioventricular node (low density).

2) L-type calcium channels(antagonists verapamil and diltiazem reduce the plateau, reduce the force of heart contraction) - cells of the atrial myocardium, the working myocardium of the ventricles, Purkinje fibers, cells of the sinatrial and atrioventricular nodes of automation.

3) Potassium channels
a) abnormal straightening(fast repolarization): atrial myocardial cells, working ventricular myocardium, Purkinje fibers
b) Delayed straightening(plateau) cells of the atrial myocardium, working ventricular myocardium, Purkinje fibers, cells of the sinatrial and atrioventricular nodes of automation
in) generating I-current, transient outgoing current of Purkinje fibers.

4) "Pacemaker" channels that form I f - the incoming current activated by hyperpolarization are found in the cells of the sinus and atrioventricular node, as well as in the cells of the Purkinje fibers.

5) Ligand-dependent channels
a) acetylcholine-sensitive potassium channels are found in the cells of the sinatrial and atrioventricular nodes of automation, cells of the atrial myocardium
b) ATP-sensitive potassium channels are characteristic of the cells of the working myocardium of the atria and ventricles
c) calcium-activated non-specific channels are found in the cells of the working myocardium of the ventricles and Purkinje fibers.

Action potential phases.

A feature of the action potential in the heart muscle is a pronounced plateau phase, due to which the action potential has such a long duration.

1): The "plateau" phase of the action potential. (feature of the excitation process):

Myocardial AP in the ventricles of the heart lasts 300-350 ms (in skeletal muscle 3-5 ms) and has an additional "plateau" phase.

PD starts with rapid depolarization of the cell membrane(from - 90 mV to +30 mV), because fast Na-channels open and sodium enters the cell. Due to the inversion of the membrane potential (+30 mV), fast Na-channels are inactivated and sodium flow stops.

By this time, slow Ca-channels are activated and calcium enters the cell. Due to the calcium current, depolarization continues for 300 ms and (unlike skeletal muscle) a “plateau” phase is formed. Then the slow Ca-channels are inactivated. Rapid repolarization occurs due to the release of potassium ions (K+) from the cell through numerous potassium channels.

2) Long refractory period (a feature of the excitation process):

As long as the plateau phase continues, sodium channels remain inactivated. Inactivation of fast Na-channels makes the cell non-excitable ( absolute refractoriness phase, which lasts about 300 ms).

3) Tetanus in the heart muscle is impossible (feature of the contraction process):

The duration of the absolute refractory period in the myocardium (300 ms) coincides with the duration of the reduction(ventricular systole 300 ms), therefore, during systole, the myocardium is unexcitable, does not respond to any additional stimuli; summation of muscle contractions in the heart in the form of a tetanus is impossible! The myocardium is the only muscle in the body that always contracts only in single contraction mode (contraction is always followed by relaxation!).