Myocardial ischemia has traditionally been characterized as an imbalance between energy supply and demand. In the initial seconds after a sudden reduction of coronary blood flow, myocardial energy demand most certainly exceeds the reduced energy supply. This temporary mismatch, however, is an inherently unstable condition because regional contractile dysfunction ensues. The mechanisms responsible for the rapid reduction in contractile function of the acutely ischemic myocardium are still poorly understood. If some residual blood flow exists, a state of "perfusion-contraction matching" can be maintained without the development of irreversible damage. The metabolic status of such hypoperfused myocardium improves as myocardial lactate production is attenuated and creatine phosphate, after an initial reduction, returns towards control values. The hypoperfused myocardium can respond to inotropic stimulation by dobutamine with increased function. The recruitment of an inotropic reserve implies increased energy utilization. In fact, the partially normalized lactate production is again increased, and creatine phosphate is decreased again. Apparently, the inotropic challenge once again precipitates a supply-demand imbalance which had been at least partially corrected by the ischemia-induced decrease of regional contractile function. A situation of chronic contractile failure in viable myocardium which normalizes upon reperfusion has been termed myocardial "Hibernation". Myocardial "Stunning" is characterized by a reversible post-ischemic contractile dysfunction despite full restoration of blood flow. The underlying mechanisms are not clear in detail. An inadequate energy supply and an impaired sympathetic neurotransmission have been excluded. Potential mechanisms, which are not mutually exclusive, may include (1) damage of membranes and enzymes by free radicals, (2) an increase in free cytosolic calcium during ischemia and reperfusion, and (3) a decrease of the calcium sensitivity of the myofibrils. The equally pronounced increases in regional contractility in normal and "stunned" myocardium during intracoronary calcium infusion, postextrasystolic potentiation and the infusion of the calcium-sensitizing agent AR-L-57, however, suggest an unchanged calcium sensitivity of reperfused myocardium. Interventions to reduce free radical formation or to increase their elimination attenuate myocardial stunning. Likewise, pretreatment with calcium antagonists before ischemia attenuates myocardial stunning. This effect is probably related to an attenuated myocardial calcium overload during early ischemia. The potential benefit from calcium antagonists when given after established reperfusion remains controversial.(ABSTRACT TRUNCATED AT 400 WORDS)