CORONARY CIRCULATION (circulatio coronaria; lat. coronarius coronal; synonym coronal blood circulation) — the movement of blood on coronary (coronal) vessels of heart providing delivery of oxygen and nutritious substrates to all tissues of heart and washing away of products of metabolism from them.
The myocardium is hit blood on two coronal arteries — right and left which mouths are located in a root of an aorta at shutters of the aortal valve. These are vessels of muscular type. Branches of the left coronal artery supply with blood a left ventricle, an interventricular partition, the left and partially right auricle. Branches of the right coronal artery supply walls of the right half of heart. Such scheme of blood supply of heart is observed not in all cases (see. Heart ), what matters for localization and the sizes of the centers of a necrosis at obstruction of different branches of coronary arteries (see. Myocardial infarction ). Large trunks of an artery, creeping on the surface of heart, give the branches leaving deep into at right angle; branchings reach eight orders. Coronary arteries carry to arteries of trailer type, however they have the interarterial anastomosis capable to miss from 3 to 5% of a blood-groove in the pool of their arrangement. Growth of an interarterial anastomosis and increase in their capacity are promoted by a long hypoxia of a myocardium. The capillary network of a myocardium is very dense: the number of capillaries is close to number of muscle fibers. In a subendocardial layer the network of capillaries is more dense, than in subepicardial. The venous system of heart has complex structure. The largest vein — a coronary sine in which a venous blood from different departments of heart merges falls into the right auricle (preferential from walls of a left ventricle). Besides, small veins of heart directly fall into cavities of the right half of heart. The myocardium is penetrated by network of so-called not vascular channels. On diameter they correspond to venules and arterioles, and on a structure of a wall remind capillaries. These are tebeziyeva (vyessenova) vessels — arteriolo-, veno-and the sinolyuminalny ways connecting the corresponding vessels to cardial cavities. The sinusoids which are located in deep layers of a myocardium also belong to drainage system of heart. In them capillaries open. Structurally functional features of this system are that that they facilitate bystry dumping of a venous blood. The question of existence in heart of an arteriovenous anastomosis is discussed. An opportunity funkts, «shuntings» — a preferential blood-groove on any preferable piece of a coronary bed is supposed. However opinion on a role To. to. as the additional «waste» circle of blood circulation is not confirmed. Coronal vessels are plentifully supplied with sympathetic and parasympathetic nerves. Also capillaries are innervated.
Intensity To. to. normal depends on the need of heart for oxygen, edges it is very high and it is characterized by consumption of 6 — 8 ml of oxygen in 1 min. on 100 g of weight of heart in the conditions of rest of an organism. The cardiac muscle has ability as much as possible to extract oxygen from the inflowing blood: a coronary venous blood contains 5 — 7 about. % of oxygen, whereas blood from venas cava — 14 — 15 about. %. Thereof any increase in energy balance during the strengthening of cardiac performance is provided with oxygen due to increase in rate of volume flow of a coronary blood-groove, edges at rest are made by 60 — 80 ml in 1 min. on 100 g of weight of heart. The gain of a blood-groove results from expansion of coronary vessels, opening of capillaries, and also owing to raising of the ABP. Therefore, in the conditions of rest of an organism coronary vessels shall possess a high tone. It is one of features of system K. to. — a combination of a high level of basal exchange in a myocardium and a high tone of the vessels having therefore a big broad reserve which allows to increase a blood stream by 5 — 7 times at increase of cardiac performance. The gain of oxygen consumption due to strengthening of its extraction by blood has smaller value and is observed usually only at very big loads of heart.
The considerable fluctuations of inflow of blood connected with phases of a cardial cycle are characteristic of blood supply of a myocardium of a left ventricle. During a diastole about 85% of blood inflow, and during a systole — 15%. For a myocardium of a right ventricle a systolic and diastolic phase K. to. differ a little. Staging To. to. it is caused by the fact that forces of extravasated compression in walls of a left ventricle during a systole create an obstacle for course of blood in the pool of the left coronary artery (fig).
Normal at increase of heartbeat of discrepancy between the increased need of heart for oxygen and capacity of vessels does not arise at the expense of active vasodilatation under the influence of metabolic factors. At the same time extravasated compression by hemodynamically inefficient extrasystoles reduces To. to. Systolic compression of a myocardium promote outflow of a venous blood; at each systole blood gushes forth from a coronary sine. There are data that throughout a coronary bed there is no site of a steady flow of blood: in capillaries it moves also unevenly with a maximum of speed in a phase of a systole.
Questions of coronary microcirculation are developed insufficiently owing to great technical difficulties. Due to the existence in walls of heart of the intramural pressure increasing towards inner layers, the vessels located in a subendocardium experience the greatest compression. At the same time subendocardial layers of a myocardium test the bigger tension and respectively big oxygen requirement. It is compensated by more dense vascularization of a subendocardium, existence of bigger number opened (functioning) capillaries what provides a bigger blood stream here during a diastole. In general the relation of subendocardial) to subepicardial is normal of a blood-groove more unit. Vessels with initially reduced tone lose ability to reactions of self-control, becoming passive tubes, and their exposure to extravasated compression increases. In these conditions (exhaustion of a broad reserve) at increase in a cardiac rhythm To. to. will not increase, it can even decrease.
Many facts testify to the myogenetic nature of a high tone of coronary vessels normal and to close connection of myogenetic and metabolic mechanisms of its regulation. In the standard opinion, as a link between cardiac performance and a coronary blood-groove serve the changes of power metabolism in a cardiac muscle having vasodilating effect. The most power-intensive cardiac performance at tachycardia is considered (in comparison with a consumption of oxygen on cardiac performance at the raised ABP and at a high stroke output). Expansion of coronary vessels happens also at a lack of oxygen. There is an opinion that the hypoxia is perceived by a myocardium in the same way, as well as increase in oxygen requirement during the strengthening of cardiac performance, i.e. mechanisms of a functional and reactive hyperemia admit in essence identical. According to this point of view, reaction of coronary vessels is defined only by a ratio blood stream/exchange regardless of whether delivery of oxygen at the changed requirement changes or oxygen requirement changes. However specific mechanisms of working and reactive giperemiya, apparently, are various that is caused by incomparable metabolic rates in that and other case. Also properties of a vascular wall at a hypoxia are not comparable and at functional congestion, though in that, and in other case vasodilatation takes place: in the first case coronary vessels become passive tubes, easily deformable forces of extravasated compression, and in the second — extending, they do not lose the elastic properties. There is an opinion that expansion of coronal vessels at a hypoxia can depend on direct influence of a lack of oxygen on unstriated muscles, however direct proofs of it very little. Are suggested that the anoxemia changes sensitivity of unstriated muscles of vessels to action of the metabolites appearing in the conditions of a hypoxia. The most reasoned is considered the hypothesis of adenosine regulation To. to., according to a cut the lack of oxygen is followed by the accelerated disintegration of ATP, and products of this disintegration — adenosine, inosine, hypoxanthine — possess strong coronarodilator action. This hypothesis does not explain the mechanism of functional congestion since during the strengthening of cordial activity of decomposition products of adenosine it is not revealed. The metabolic theory of regulation To. to. considers, in addition to ATP decomposition products, other factors of the humoral nature: potassium, intermediata of a tricarbonic acid cycle, products of anaerobic exchange, change of an osmotichnost of an intercellular lymph, inorganic phosphate. However attempts to reproduce vascular reactions by introduction to a coronary bed of this or that substance did not yield the results matching natural reactions. It is possible that vasodilatation both at reactive, and at functional congestion represents result of the unidirectional action of a number of factors. Coronarodilator action A1 and E1 prostaglandins in pharmakol possess. doses. They can take part in a koronarodilatation during the strengthening of cardiac performance. Kinina also expand coronary vessels. Carry angiotensin, Pituitrinum to koronarokonstriktorny humoral factors. The coronary vazodilatation during the strengthening of cardiac performance can be explained by means of the gistomekhanichesky hypothesis made by V. M. Hayutin of rather functional congestion of skeletal muscles: reduction of muscle fiber deforms a vessel so that automatic rhythmics of smooth muscle elements of its wall is suppressed and there is a vazodilatation.
Nervous control To. to. in many respects remains not until the end of investigated. Even in an experiment it is difficult to separate primary vasculomotor action of nerves from secondary, mediated through change kardio-and a hemodynamics, metabolism of a myocardium. Irritation of c. gave to N of page (kernels of a hypothalamus) at animals various reactions of coronary vessels. At dogs with denervated heart coronary vasomotor reaction stepped on emotional loading considerably later and not so quickly stopped at abirritation, as at the kept innervation. Possibly, in bystry and adequate adaptation K. to. to the current requirements of heart the main regulating role of interaction of natural sympathetic and parasympathetic nervous influences on coronary vessels consists. By well checked experiments it is established that excitement of vagus nerves expands coronary vessels. The mediator of cholinergic nervous action — acetylcholine — also expands coronary vessels. At irritation of cordial branches of sympathetic nerves expansion of coronary vessels and increase is observed too To. to. However at the same time force and frequency of heartbeat increases, the speed of reduction of a cardiac muscle and intramural pressure — the factors changing metabolism of a myocardium that in itself is caused by expansion of coronary vessels grows. At excitement of sympathetic nerves decrease in content of oxyhemoglobin in the blood flowing from a coronary sine that bring as an indicator of an insufficient coronary vazodilatation or the hidden konstriktion of vessels is sometimes observed. Some authors observed primary increase in resistance of coronary vessels at irritation of sympathetic nerves which was replaced by a strong and long vazodilatation. At decrease in body temperature, reduction in any way of intensity of exchange the neurogenic konstriktion of coronary vessels comes to light more often and more clearly. Reactions of coronary arteries to irritation of sympathetic nerves are mediated by activation alpha and beta adrenoceptors which as believe, are located on membranes of unstriated muscles of vessels. The coronary vazodilatation at irritation of sympathetic nerves is connected with the beta and adrenergic receptor mechanism which prevails over alpha and adrenergic, responsible for a koronarokonstriktion. End reaction is defined by quantitative dominance of activation of these or those receptors. During the blocking of p-adrenergic receptors propranolol the irritation of sympathetic nerves or introduction of catecholamines causes a koronarokonstriktion of the alpha and adrenergic nature. Adrenaline usually causes long and strong expansion of coronary vessels. But at the same time also consumption at a myocardium of oxygen, and also cardiac performance strongly grows. At direct introduction of catecholamines to coronary vessels the vazodilatation precedes reaction of heart. Blocking of p-adrenergic receptors reveals a small initial design of coronary vessels at action of catecholamines. There is an opinion that a ratio and and p-adrenergic receptors in coronary vessels of different diameter variously and that this ratio can change under the influence of temperature, pharmakol, agents, etc. Thus, despite significant progress in studying of regulation To. to., many questions remain not solved yet.
At the heart of various forms of disturbance To. to. (see. Coronary insufficiency ) emergence of an imbalance between the need of a myocardium for oxygen and its delivery by blood lies. In most cases this imbalance arises owing to obstructive defeats of coronary vessels atherosclerotic process. At considerable sizes of obstruction the balance is broken already at rest — the blood stream is initially reduced. However in some cases the blood stream in a myocardium at rest normal, but during the strengthening of work or increases very little, or even decreases. The passive condition of walls of the vessels extending distalny the site of a stenosis that does them subject to compression by the reduced myocardium can be one of the possible reasons of such dynamics of a coronary blood-groove at loading. Then any increase in load of heart will limit inflow of blood. At the same time subendocardial layers of a myocardium especially suffer. Apparently, cases when the reason of discrepancy between requirement and delivery of oxygen lies in neurogenic spastic reactions of the coronary arteries which are not affected with atherosclerosis meet less often. To reduction To. to. also increased viscosity of blood increasing vascular resistance promotes. Restriction of utilization of oxygen with a myocardium can be connected with factors biochemical, the nature, napr, with disturbance of process of dissociation of hemoglobin of blood (see. Myocardial infarction , Coronary insufficiency , Stenocardia ).
See also Blood circulation .
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A. V. Trubetskoy.