The first observations on the effects of decreased blood flow on myocardial contractility were made by Tennant and Wigers in 1935 in coronary occlusion experiments [1]. The relationships between the duration and severity of the ischaemia and their functional, biochemical and structural consequences have been established much more recently only when sophisticated technology became available for application in laboratory animals It became clear, subsequently, that myocardial ischaemia rapidly causes (in seconds) severe contractile dysfunction [2] and that restoration of coronary flow is capable of reversing this effect in a manner that clearly depends on the period of duration of the ischaemia. If sufficiently brief, the contractile recovery is total but, beyond a certain time limit, reperfusion does not prevent necrosis of parts of the ischaemic myocardium and this is progressively greater the more protracted the ischaemia [3-5] and the contractile recovery is incomplete or none. A simple model was established and widely accepted in which the ischaemia would be accompanied by severe contractile dysfunction and reperfusion by contractile recovery that is assumed to be complete and more or less immediate; at least that which produced myocardial necrosis. Contractile dysfunction and necrosis would be consequences of progressive deterioration of the cellular energy status produced by the protracted anaerobic metabolism