EARLY PHASE OF MYOCARDIAL ISCHEMIC INJURY AND INFARCTION

The acute effects of ischemia on myocardial tissue are reviewed in this paper with emphasis on how the events observed in experimental myocardial ischemic injury in dogs relate to the sequential changes occurring in the myocardium of man during the first few hours after the onset of acute infarction. The general effects of ischemia on myocardium include those which are secondary to a diminished local supply of substances such as oxygen and metabolites as well as changes resulting from the impaired diffusion of substances such as lactic acid and electrolytes from the poorly perfused ischemic tissue to the general circulation. Cell death (irreversible injury) first develops after 20 minutes of ischemia in areas of maximum injury in the dog heart and infarcts are not fully developed for 60 to 120 minutes after occlusion. Prior to the development of cell death, the severely ischemic cells are reversibly injured and show a variety of alterations from normal. These changes include depletion of supplies of glycogen and high energy phosphate, increased content of lactic acid and hydrogen, relaxation of myofibrils and failure of contraction. Cells which have just died show the same changes as well as mitochondrial, electrolyte, and nuclear defects. Which, if any, of the preceding changes causes the development of irreversibility in ischemic injury remains to be established. Some data is presented in support of the hypothesis that mitochondrial defects may be critical in the genesis of the irreversible state. © 1969.