Opie L H
MRC Ischaemic Heart Disease Research Unit, Department of Medicine, University of Cape Town.
S Afr Med J. 1987 Dec 5;72(11):740-7.
Ischaemic heart disease (IHD) kills by myocardial failure or by the sudden development of lethal ventricular arrhythmias such as ventricular fibrillation. Impaired coronary flow causes myocardial ischaemia, which acutely predisposes to ventricular fibrillation. If ischaemia is sustained, it may develop into cell necrosis (myocardial infarction). All these clinical manifestations of IHD depend on myocardial metabolic changes which in turn can be modified by pharmacological manipulation such as beta-adrenergic blockade or by reperfusion. The mechanism of reperfusion injury appears to be metabolic in origin, related either to free radicals or excess accumulation of cytosolic calcium.
缺血性心脏病（IHD）可因心肌衰竭或因致命性室性心律失常（如心室颤动）的突然发作而导致死亡。冠状动脉血流受损会导致心肌缺血，这会急性诱发心室颤动。如果缺血持续存在，可能会发展为细胞坏死（心肌梗死）。IHD的所有这些临床表现都取决于心肌代谢变化，而这些变化又可以通过诸如β-肾上腺素能阻断或再灌注等药物操作来改变。再灌注损伤的机制似乎源于代谢，与自由基或胞质钙的过量积累有关。
