The heart muscle is critically dependent on energy supply from oxidative phosphorylation, which in turn requires an adequate oxygen supply. Its greatest proportion (80%) is used by mechanical work of the heart, followed by the ion pumps and protein resynthesis. Global ischaemia of the isolated heart leads within two seconds to the electron transport arrest in mitochondria and at the same time glycogenolysis, an alternative energy source, is accelerated. The content of macroergic phosphate declines rapidly, in particular that of creatine phosphate and within 10-15 seconds mechanical activity stops. The subsequent fate of ischaemic tissue depends on the degree and period of ischaemia. Very brief ischaemia (1-2 min.) does not cause any functional sequelae after restoration of the arterial blood supply. Longer ischaemia (10-15 min.) leads during reperfusion to postischaemic dysfunction (stunned myocardium, G. R. Heyndrickx) which is completely reversible. Prolonged hypoperfusion lead to mechanical dysfunction, which may last weeks and months but is reversible (hibernated myocardium--S. H. Rahimtoola). Only prolonged critical ischaemia (30-60 min. and perfusion as low as 0.15 ml/min./g tissue) leads to necrosis of muscle cells. Its development is enhanced in particular by an extensive drop of macroergic phosphates with inhibition of anaerobic glycolysis, excessive amounts Ca++ in cardiomyocytes and cumulation of catabolites, such as lactate, H+ and free radicals.

Keywords: Animals; Humans; Myocardial Ischemia /metabolism/; Myocardial Reperfusion; Myocardium /metabolism/