The myocardium

Abstract

The myocardium O VER the past few years a number of new and important concepts relating to the heart and the coronary circulation have evolved. They are relevant to the practice of anaesthesia and intensive care, and will be discussed under the headings of local vs humoral and hormonal control of the coronary circulation, effects ofischaemia on cardiac fimction, including myocardial stunning, hibernation and preconditioning and, finally, coronary steal. Control of the coronary circulationThe normal control of coronary blood flow is through alterations in the resistance of intramyocardial arterioles. Increased breakdown of ATP results in increased concentrations of adenosine, a potent endogenous vascular smooth muscle relaxant. This local mechanism allows coronary blood flow to be adjusted to the oxygen requirements.L2 Other mediators are also involved in the control of the coronary circulation. These include nitric oxide, prostacyclin, thromboxane and endothelins, s-s These mediators are synthesised and released by the endothelium. In the presence of atheroma, the endothelial function in large arteries is disrupted. Imbalances between mediators predispose to inappropriate vasoconstriction, platelet aggregation and thrombosis, 6 Endothelins may have a particular role in such events as they are among the most potent vasoconstrictors. 7Neurogenic control Activation of the sympathetic nervous system causes marked changes in coronary blood flow. These changes are mediated in part by changes in metabolic demand. However, large and small coronary arteries are subject to control by alpha-and beta-adrenergic mechanisms. Alpha l-and alphaz-adrenoceptors elicit constriction, while beta 1-and beta2-adrenoceptors elicit dilatation, of large coronary arteries, s Alphaadrenergic constriction competes with metabolic vasodilatation. This competition is attenuated by the endogenous production of adenosine. However, adenosine modulates alpha z-and not alphai-adrenoceptor mediated vasoconstriction. 9Activation of the parasympathetic nervous system usually causes a reduction in coronary blood flow because bradycardia and hypotension reduce oxygen demand. However, if the bradycardia resulting from vagal stimulation is prevented by pacing, coronary blood flow increases uniformly across the left ventricular wall in response to vagal stimulation. By contrast, acetylcholine preferentially vasodilates the vessels of the subendocardium. 1~While the role of the autonomic nervous system in the control of the coronary circulation has long been underestimated, many studies of patients with variant angina suggest that there is local nonspecific supersensitivity to vasoconstrictors. 11 Alpha-adrenergic constriction of coronary resistance vessels may result in the precipitation ofpost-stenotic myocardial ischaemia both in experimental models and in patients with effort angina. In contrast, the adverse effects of beta-adrenergic stimulation are a consequence of the tachycardia and the tachycardia-related redistribution of coronary blood flow, as t...