| Abstrakt: |
Controversies on acetylcholine-induced increases or decreases in coronary blood flow arise from obvious species differences, the role of endothelium in mediating vascular smooth muscle responses and the marked negative chronotropic and inotropic effects of acetylcholine. In man, there appears to be a predominant dilation of intact epicardial coronary arteries and a constriction of atherosclerotic segments. However, at present there is no evidence for a vagal initiation of myocardial ischaemia.Coronary vascular β-receptors mediate dilation, but appear to be functionally insignificant during sympathetic activation. The β-adrenergic mechanisms contributing to myocardial ischaemia are indirect, mediated by a tachycardia-related redistribution of blood flow away from the ischaemic myocardium, α-receptors mediating epicardial coronary artery constriction in experimental studies appear not to be responsible for the initiation of ischaemia in patients with angina at rest. However, α-adrenergic constriction of coronary resistance vessels resulting in the precipitation of poststenotic myocardial ischaemia was demonstrated in experimental studies and recently confirmed in patients with effort angina. [ABSTRACT FROM PUBLISHER] |
