When severely ischemic myocardium is reperfused, prolonged myocardial dysfunction--a phenomenon named myocardial stunning--frequently occurs. Stunning also occurs in a variety of other situations. These include myocardium located adjacent to infarcted tissue, transient increase in myocardial O2 demands in the presence of incomplete coronary obstruction, during both systole and diastole, in isolated perfused hearts rendered ischemic or anoxic, and in a variety of clinical situations, such as following ischemic arrest in cardiac surgery, thrombolytic reperfusion, and after episodes of severe ischemia in Prinzmetal's angina or unstable angina. Although the fundamental mechanism(s) responsible for myocardial stunning has not been elucidated, in experimental preparations calcium antagonists, free-radical scavengers, and neutrophil depletion have each been found to be helpful in minimizing it.