title: Myocardial ischaemia--metabolism and its modification.
abstract: 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.
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000378:metabolism; D003327:Coronary Disease / Q000145:classification; D006168:Guinea Pigs; D006801:Humans; D007511:Ischemia / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D014693:Ventricular Fibrillation / Q000378:metabolism
chemical_list: D000319:Adrenergic beta-Antagonists