Сигналы управления могут реализовываться непосредственно исполнительным звеном регулятора. В частности, эфферентные нейроны сердечно-сосудистого центра могут передавать управляющие сигналы непосредственно к объекту управления, сердцу и кровеносным сосудам. Сигналы управления могут реализовываться опосредованно. В частности, управляющие сигналы нервной системы могут реализовываться через определенные химические вещества (гуморальные активные вещества) гуморальным путем, посредством предварительного транспорта этих веществ с жидкостями организма к объектам управления. Так могут действовать гормоны желез внутренней секреции. Железы внутренней секреции выполняют здесь функцию промежуточных исполнительных звеньев регулятора. В совокупности они являются системой исполнительных органов регуляторов нервной системы. В ответ на нервные сигналы эндокринные железы выделяют гормоны, транспортируемые с кровью к объектам управления (органам-мишеням, клеткам-мишеням).
     Структура, функции и механизмы управления в системе кровообращения соответствуют принципу иерархии структур, функций и механизмов управления в системах организма.
     Классификация механизмов управления в системе кровообращения - это описание систематизированных представлений об иерархии механизмов управления.
     Принципы управления в системе кровообращения соответствуют наиболее вероятным общим представлениям о законах управления в живых системах (Трифонов Е.В., 1980).
     Методологией исследования управления в системе кровообращения, адекватной её вероятностной сущности является вероятностная методология с её аксиомами и принципами (Трифонов Е.В., 1978,..., ..., 2014, …). EXERCISE Body_ID: HC024001 The cardiovascular adjustments that take place during exercise consist of a combination of neural and local (chemical) factors. The neural factors include (1) central command, (2) reflexes that originate in the contracting muscle, and (3) the baroreceptor reflex. Body_ID: P024004 Central command is the cerebrocortical activation of the sympathetic nervous system that produces cardiac acceleration, increased myocardial contractile force, and peripheral vasoconstriction. Reflexes are activated intramuscularly by stimulation of mechanoreceptors (by stretch, tension) and chemoreceptors (by products of metabolism) in response to muscle contraction. Impulses from these receptors travel centrally via small myelinated (group III) and unmyelinated (group IV) afferent nerve fibers. The group IV unmyelinated fibers may represent the muscle chemoreceptors, as no morphological chemoreceptor has been identified. The central connections of this reflex are unknown, but the efferent limb consists of sympathetic nerve fibers to the heart and peripheral blood vessels. The baroreceptor reflex is described in Chapter 21, and the local factors that influence skeletal muscle blood flow (metabolic vasodilators) are described in Chapter 23. Vascular chemoreceptors are important in the regulation of the cardiovascular system during exercise. Evidence for this assertion comes from the observations that the pH, Pco2, and Po2 of arterial blood remain normal during exercise, and that the vascular chemoreceptors are located on the arterial side of the circulatory system. Body_ID: P024005 Mild to Moderate Exercise Body_ID: HC024002 In humans or trained animals, anticipation of physical activity inhibits the vagal nerve impulses to the heart and increases sympathetic discharge. The simultaneous inhibition of parasympathetic areas and activation of sympathetic areas of the medulla increase heart rate and myocardial contractility. The tachycardia and enhanced contractility increase cardiac output. Body_ID: P024006 Peripheral resistance. Body_ID: HC024003 When cardiac stimulation occurs, the sympathetic nervous system also changes vascular resistance in the periphery. In skin, kidneys, splanchnic regions, and inactive muscle, sympathetic-mediated vasoconstriction increases vascular resistance, and thereby diverts blood away from these areas (Fig. 24-1). This increased vascular resistance persists throughout the period of exercise. Body_ID: P024007 As cardiac output and blood flow to active muscles increase with progressive increases in the intensity of exercise, visceral blood flow (i.e., to the splanchnic and renal vasculatures) decreases. Blood flow to the myocardium increases, whereas flow to the brain is unchanged. Skin blood flow initially decreases during exercise, and then it increases as body temperature rises with increments in the duration and intensity of exercise. Skin blood flow finally decreases when the skin vessels constrict as total body O2 consumption nears its maximal value (Fig. 24-1). The major circulatory adjustment to prolonged exercise occurs in the vasculature of the active muscles. Local formation of vasoactive metabolites dilates the resistance vessels markedly. This dilation progresses with increases in the intensity of exercise. Potassium is one of the vasodilator substances released by the contracting muscle, and this ion may be partly responsible for the initial decrease in vascular resistance in the active muscles. Other contributing factors may be the release of adenosine and a decrease in tissue pH during sustained exercise. The local accumulation of metabolites relaxes the terminal arterioles. As a result, blood flow through the muscle may increase 15-fold to 20-fold above the resting level. This metabolic vasodilation of the precapillary vessels in active muscles occurs very soon after the onset of exercise. The decrease in total peripheral resistance (TPR) enables the heart to pump more blood at a lesser load and it pumps more efficiently than if TPR were unchanged (see Chapters 22 and 23). Marked changes in the capillary circulation also occur during exercise. Only a small percentage of the capillaries are perfused at rest, whereas in actively contracting muscle, all or nearly all of the capillaries contain flowing blood (capillary recruitment). The surface area available for exchange of gases, water, and solutes is increased many times. Furthermore, the hydrostatic pressure in the capillaries is increased because of the relaxation of the resistance vessels. Hence, water and solutes move into the muscle tissue. Tissue pressure rises and remains elevated during exercise as fluid continues to move out of the capillaries; this tissue fluid is carried away by the lymphatics. Lymph flow is increased as a result of the rise in capillary hydrostatic pressure and of the massaging effect of the contracting muscles on the valve-containing lymphatic vessels (see Fig. 23-11). Body_ID: P024011 Contracting muscle avidly extracts O2 from the perfusing blood and thereby increases arteriovenous O2 difference (Fig. 24-2). This release of O2 from the blood is facilitated by the shift in the oxyhemoglobin dissociation curve during exercise. During exercise, the high concentration of CO2 and the formation of lactic acid reduce the tissue pH. This decrease in pH plus the increase in temperature in the contracting muscle shifts the oxyhemoglobin dissociation curve to the right (see Chapter 28). Therefore, at any given partial pressure of O2, less O2 is held by the hemoglobin in the red cells, and consequently more O2 is available for the tissues. Oxygen consumption may increase as much as sixtyfold, with only a fifteenfold increase in muscle blood flow. Muscle myoglobin may serve as a limited O2 store during exercise, and it can release the attached O2 at very low partial pressures. However, the myoglobin can also facilitate O2 transport from capillaries to mitochondria by serving as an O2 carrier. Body_ID: P024013 Cardiac output. Body_ID: HC024004 page 434 page 435 Body_ID: P0435 Because the enhanced sympathetic drive and the reduced parasympathetic inhibition of the sinoatrial node continue during exercise, tachycardia persists. If the workload is moderate and constant, the heart rate will reach a certain level and remain there throughout the period of exercise. However, if the workload increases, the heart rate increases concomitantly until a plateau of about 180 beats/min is reached during strenuous exercise. In contrast to the large increase in heart rate, the increase in stroke volume is only about 10% to 35%, the larger values occurring in trained individuals (Fig. 24-2). In well-trained distance runners, whose cardiac outputs can reach six to seven times the resting level, stroke volume reaches about twice the resting value. Body_ID: P024014 Thus, the increase in cardiac output observed during exercise is correlated principally with an increase in heart rate. If the baroreceptors are denervated, the cardiac output and heart rate responses to exercise are small compared with those in animals with normally innervated baroreceptors. However, in dogs with total cardiac denervation, exercise still increases cardiac output as much as it does in normal animals. This increase in cardiac output is achieved chiefly by means of an elevated stroke volume. However, if a ?-adrenergic receptor antagonist is given to the dogs with denervated hearts, exercise performance is impaired. The ?-adrenergic receptor blocker apparently prevents the cardiac acceleration and enhanced contractility caused by increased amounts of circulating catecholamines. Therefore, the increase in cardiac output necessary for maximal exercise performance is limited. Body_ID: P024015 Venous return. Body_ID: HC024005 In addition to the contribution made by sympathetically mediated constriction of the capacitance vessels in both exercising and nonexercising parts of the body, venous return is aided by the auxillary pumping action of the working skeletal muscles and the muscles of respiration (see also Chapter 22). The intermittently contracting muscles compress the veins that course through them. Because the venous valves are oriented toward the heart, the contracting muscle pumps blood back toward the right atrium (see Chapter 23). In exercise, the flow of venous blood to the heart is also aided by the deeper and more frequent respirations that increase the pressure gradient between the abdominal and thoracic veins (intrathoracic pressure becomes more negative during exercise). Body_ID: P024016 In humans, blood reservoirs do not contribute much to the circulating blood volume. In fact, blood volume is usually reduced slightly during exercise, as evidenced by a rise in the hematocrit ratio. This decrease in blood volume is caused by water loss externally through sweating and enhanced ventilation, and by fluid movement into the contracting muscle. Body_ID: P024017 However, fluid loss is counteracted in several ways. The fluid loss from the vascular compartment into the contracting muscles eventually reaches a plateau as the interstitial fluid pressure rises and opposes the increased hydrostatic pressure in the capillaries of the active muscle. Fluid loss is partially offset by movement of fluid from the splanchnic regions and inactive muscle into the bloodstream. This influx of fluid results (1) from the decrease of hydrostatic pressure in the capillaries of these tissues, and (2) from an increase in the plasma osmolarity, because of movement of osmotically active molecules into the blood from the contracting muscle. In addition, reduced urine formation by the kidneys helps to conserve body water. Body_ID: P024018 The large volume of venous blood returning to the heart is so effectively pumped through the lungs and out into the aorta that central venous pressure remains essentially constant. Thus, the Frank-Starling mechanism of a greater initial fiber length does not account for the greater stroke volume in moderate exercise. X-ray films of individuals at rest and during exercise reveal a decrease in heart size during exercise. However, during maximal or near-maximal exercise, right atrial pressure and end-diastolic ventricular volume do increase. Thus, the Frank-Starling mechanism contributes to the enhanced stroke volume in very vigorous exercise. Body_ID: P024019 Arterial pressure. Body_ID: HC024006 If the exercise involves a large proportion of the body musculature, such as in running or swimming, the reduction in total vascular resistance can be considerable. Nevertheless, arterial pressure starts to rise with the onset of exercise, and the increase in blood pressure roughly parallels the severity of the exercise performed (Fig. 24-2). Therefore, the increase in cardiac output is proportionally greater than the decrease in TPR. The vasoconstriction produced in the inactive tissues by the sympathetic nervous system (and to some extent by the release of catecholamines from the adrenal medulla) is important for maintenance of normal or increased blood pressure. Sympathectomy or drug-induced block of the adrenergic sympathetic nerve fibers decreases the arterial pressure (hypotension) during exercise. Body_ID: P024020 Sympathetic neural activity also elicits vasoconstriction in active skeletal muscle when additional muscles are recruited. In experiments in which one leg is working at maximal levels and then the other leg starts to work, blood flow decreases in the first working leg. Furthermore, blood levels of norepinephrine rise significantly during exercise, and most of the norepinephrine is released from the sympathetic nerves to the active muscles. Body_ID: P024021 As body temperature rises during exercise, the skin vessels dilate in response to thermal stimulation of the heat-regulating center in the hypothalamus, and the TPR decreases further. This reduction in TPR would reduce blood pressure were it not for the increased cardiac output and the constriction of arterioles in the renal, splanchnic, and other tissues. Body_ID: P024022 page 435 page 436 Body_ID: P0436 In general, the mean arterial pressure rises during exercise as a result of the increase in cardiac output. However, the effect of enhanced cardiac output is offset by an overall decrease in TPR, and therefore the mean blood pressure increases only slightly. Vasoconstriction in the inactive vascular beds helps to maintain a normal arterial blood pressure for adequate perfusion of the active tissues. The actual mean arterial pressure attained during exercise thus represents a balance between cardiac output and TPR (see Chapter 19). Systolic pressure usually increases more than diastolic pressure, which results in an increase in pulse pressure (Fig. 24-2). The larger pulse pressure is primarily attributable to a greater stroke volume, but also to a more rapid ejection of blood by the left ventricle and a diminished peripheral runoff during the brief ventricular ejection period (see also Chapters 16 and 19). Body_ID: P024023 Severe Exercise Body_ID: HC024007 During exhaustive exercise, the compensatory mechanisms begin to fail. Heart rate attains a maximal level of about 180 beats/min, and stroke volume reaches a plateau. The heart rate may then decrease, resulting in a fall in blood pressure. The subject also frequently becomes dehydrated. Sympathetic vasoconstrictor activity supersedes the vasodilator influence on the vessels of the skin. However, vasoconstriction of skin vessels also decreases the rate of heat loss. Body temperature is normally elevated in exercise. Reduction in heat loss through cutaneous vasoconstriction can lead to very high body temperatures and to acute distress during severe exercise. The tissue and blood pH decrease as a result of increased lactic acid and CO2 production. The reduced pH is probably the key factor that determines the maximal amount of exercise a given individual can tolerate. Muscle pain, a subjective feeling of exhaustion, and a loss of will to continue determine the exercise tolerance. A summary of the neural and local effects of exercise on the cardiovascular system is diagrammed in Fig. 24-3. Body_ID: P024024 Postexercise Recovery Body_ID: HC024008 Body_ID: P024026 When exercise stops, heart rate and cardiac output abruptly decrease-the sympathetic drive to the heart is essentially removed. In contrast, TPR remains low for some time after the exercise is stopped, presumably because of the accumulation of vasodilator metabolites in the muscles during the exercise period. As a result of the reduced cardiac output and persistence of vasodilation in the muscles, arterial pressure falls, often below preexercise levels, for brief periods. Blood pressure is then stabilized at normal levels by the baroreceptor reflexes. Body_ID: P024025 Limits of Exercise Performance Body_ID: HC024009 The two main factors that limit skeletal muscle performance in the human body are the rate of O2 utilization by the muscles and the O2 supply to the muscles. O2 usage by muscle is probably not a critical factor. During exercise, maximal O2 consumption (&Vdot;O2max) by a large percentage of the body muscle mass is unchanged or increases only slightly when additional muscles are activated. In fact, during exercise of a large muscle mass, as in vigorous bicycling, the addition of bilateral arm exercise without change in the cycling efforts produces only a small increase in cardiac output and &Vdot;O2max However, the additional arm exercise decreases blood flow to the legs. This centrally mediated (baroreceptor reflex) vasoconstriction during maximal cardiac output prevents the fall in blood pressure that would otherwise be caused by metabolically induced vasodilation in the active muscle. If muscle O2 usage were a significant limiting factor, recruitment of more contracting muscles would use much more O2 to meet the enhanced O2 requirements. Body_ID: P024027 page 436 page 437 Body_ID: P0437 Limitation of O2 supply could be caused by inadequate oxygenation of blood in the lungs or limitation of the supply of O2-laden blood to the muscles. Failure to fully oxygenate blood by the lungs can be excluded, because even with the most strenuous exercise at sea level, arterial blood is fully saturated with O2. Therefore, O2 delivery to the active muscles (or blood flow, because arterial blood O2 content is normal) appears to be the limiting factor in muscle performance. This limitation could be caused by the inability to increase cardiac output beyond a critical level. In turn, this inability is caused by a limitation of stroke volume, because heart rate reaches maximal levels before &Vdot;O2max is reached. Hence, the major factor that limits muscle performance is the pumping capacity of the heart. Body_ID: P024028 During exercise of a small group of muscles, such as those found in the hand, the limiting factor is unknown, but it appears to lie within the muscle. Body_ID: P024029 Physical Training and Conditioning Body_ID: HC024010 The response of the cardiovascular system to regular exercise is to increase its capacity to deliver O2 to the active muscles and to improve the ability of the muscle to utilize O2. The &Vdot;O2max varies with the level of physical conditioning. Training progressively increases the &Vdot;O2max, which reaches a plateau at the highest level of conditioning. Highly trained athletes have a lower resting heart rate, a greater stroke volume, and a lower peripheral resistance than they had before training or after deconditioning. The low resting heart rate is caused by a higher vagal tone and a lower sympathetic tone. During exercise, the maximal heart rate of the trained individual is the same as that in the untrained, but it is attained at a higher level of exercise. Body_ID: P024030 The trained person also exhibits a low vascular resistance in the muscles. For example, if an individual exercises one leg regularly over an extended time and does not exercise the other leg, the vascular resistance is lower and the &Vdot;O2max is higher in the "trained" leg than in the "untrained" leg. Physical conditioning is also associated with greater extraction of O2 from the blood (greater arteriovenous O2 difference) by the muscles. With long-term training, capillary density in skeletal muscle increases. Also, an increase in the number of arterioles may account for the decrease in muscle vascular resistance. The numbers of mitochondria increase, as do the oxidative enzymes in the mitochondria. In addition, the levels of ATPase activity, myoglobin, and enzymes involved in lipid metabolism increase in response to physical conditioning. Body_ID: P024031 Endurance training, such as running or swimming, increases left ventricular volume without increasing left ventricular wall thickness. In contrast, strength exercises, such as weight lifting, increase left ventricular wall thickness (hypertrophy) with little effect on ventricular volume. However, this increase in wall thickness is small relative to that observed in chronic hypertension, in which afterload is persistently elevated because of high peripheral resistance.

См. в отдельных окнах:

УПРАВЛЕНИЕ КРОВООБРАЩЕНИЕМ ПРИ ФИЗИЧЕСКИХ НАГРУЗКАХ: ИЛЛЮСТРАЦИИ - 1
1. Схема. c. 434 = Figure 24-1 Approximate distribution of cardiac output at rest and at different levels of exercise up to the maximal O2 consumption (&Vdot;O2max) in a normal young man. (Redrawn from Ruch HP, Patton TC: Physiology and biophysics, ed 12, Philadelphia, 1974, WB Saunders.) Berne R.M., Levy M.N., Koeppen B.M., Stanton B.A. Physiology = Физиология. 8th ed. 2004, 1024 p. = 2_62/Physiology_Bern_5ed_2004.CHM.
2. Схема. Figure 24-2 Effect of different levels of exercise on several cardiovascular variables. (Data from Carlsten A, Grimby G: The circulatory response to muscular exercise in man, Springfield, Ill, 1966, Charles C Thomas.)
3. Схема. Figure 24-3 Cardiovascular adjustments in exercise. VR, Vasomotor region; C, vasoconstrictor activity; D, vasodilator activity; IX, glossopharyngeal nerve; X, vagus nerve, +, increased activity, -, decreased activity..
4. Схема. c 423 Figure 23-11 Action of the muscle pump in venous return from the legs. A, Standing at rest, the venous valves are open and blood flows upward toward the heart by virtue of the pressure generated by the heart and transmitted through the capillaries to the veins from the arterial side of the vascular system (vis a tergo). B, Contraction of the muscle compresses the vein so that the increased pressure in the vein drives blood toward the thorax through the upper valve and closes the lower valve in the uncompressed segment of the vein just below the point of muscular compression. C, Immediately after muscle relaxation, the pressure in the previously compressed venous segment falls and the reversed pressure gradient causes the upper valve to close. The valve below the previously compressed segment opens because pressure below it exceeds that above it. The segment then fills with blood from the foot. As blood flow continues from the foot, the pressure in the previously compressed segment rises. When it exceeds the pressure above the upper valve, this valve opens and continuous flow occurs as in A..
5. Схема. Figure 23-12 Evidence for participation of the muscle vascular bed in vasoconstriction and vasodilation mediated by the carotid sinus baroreceptors after common carotid artery occlusion and release. In this preparation, the sciatic and femoral nerves constituted the only direct connection between the hind leg muscle mass and the rest of the dog. The muscle was perfused by blood at a constant pressure that was completely independent of the animal's arterial pressure. (Redrawn from Jones RD, Berne RM: Am J Physiol 204:461, 1963.)
6. Схема. Figure 14–1. A. Graphs of the hemodynamic responses to dynamic exercise. B. Sequence of physiological responses to dynamic exercise. Chapter 14. ECG Exercise Testing. In: Fuster V., Alexander R.W., O'Rourke R.A., et all, Eds. Hurst's The Heart, 2-Vol Set, 10th ed. McGraw-Hill Professional, 2000, 2258 p. = 2_79/Heart12ed2007.CHM
7. Схема. Средства управления диаметром кровеносных сосудов. Механизмы тонуса, расширения и сужения сосудов.

МИКРОГЕМАЦИРКУЛЯЦИЯ: ИЛЛЮСТРАЦИИ
1. Схема. Микрогемациркуляторное русло.
2. Схема. Миогенный ответ кровеносного сосуда на повышение интрамурального давления.
3. Схема. Миогенный ответ кровеносного сосуда на понижение интрамурального давления.
4. Схема. Миогенный механизм регулирования кровотока
5. Схема. Последовательность процессов, лежащих в основе миогенного ответа.
6. Схема. Гипотеза вторичного переносчика информации в клетку.
7. Схема. Механизмы передачи управляющих сигналов к объектам управления системы кровообращения.
8. Схема. Относительная чувствительность различных сегментов микрогемациркуляторной сети к различным воздействям.