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European Heart Journal 1991 12(Supplement F):99-106; doi:10.1093/eurheartj/12.suppl_F.99
Copyright © 1991 by the European Society of Cardiology.
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© 1991 The European Society of Cardiology

Control of coronary vasomotor tone in ischaemic myocardium by local metabolism and neurohumoral mechanisms

G. Heusch

Abteilung für Pathophysiologie, Zentrum für Innere Medizin, Universitätsklinikum Essen Germany

Correspondence: Prof. Dr. Gerd Heusch, Abteilung für Pathophysiologie, Zentrum für Innere Median, Universitätsklinikum Essen, HufelandstraBe 55, 4300 Essen, Germany

There is no doubt that under normal conditions powerful local metabolic regulation adjusts coronary blood flow to myocardial oxygen consumption. However, despite substantial experimental efforts the responsible mediators are still largely unknown. Adenosine, a purported mediator of local metabolic control of coronary blood flow, is probably only involved in transient flow adaptations but not in steady state coronary autoregulation. Even below the autoregulatory range a substantial vasodilator reserve persists, and recruitment of such a vasodilator results in improved regional myocardial blood flow and attenuated regional ischaemic dysfunction.

β-adrenergic coronary dilation is of minor functional importance, {alpha}-adrenergic coronary constriction acts to attenuate increases in coronary blood flow during sympathetic activation under normal conditions, so that myocardial oxygen extraction increases to match the increased oxygen consumption, {alpha}-adrenergic coronary constriction remains operative in ischaemic myocardium, thus precipitating or contributing to acute myocardial ischaemia during sympathetic activation and exercise in experimental animals, as well as in patients with stable angina. The vagal transmitter acetylcholine-upon exogenous intracoronary infusion-induces critical constriction of epicardial coronary arteries with endothelial dysfunction and atherosclerosis. However, a vagal initiation of coronary spasm or myocardial ischaemia has not been documented so far. Similarly, peptide hormones/transmitters such as NPY, vasopressin and angiotensin can induce myocardial ischaemia upon exogenous administration. Their pathophysiological role in myocardial ischaemia, however, remains to be established.

Key Words: Coronary vasomotor tone • myocardial ischaemia • coronary reserve • ar-adrenoceptors • ACE-inhibitors


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