Abstract
Periods of severe ischemia of 15 minutes or less injure myocytes of the dog heart reversibly in that reperfusion of the affected tissue with arterial blood salvages all myocytes destined to die if the ischemia is not relieved. While the myocytes are ischemic, they develop numerous changes as a consequence of ischemic metabolism including depletion of P and accumulation of glycolytic intermediates, H+, and the endproducts of adenine nucleotide pool degradation. With restoration of arterial flow, aerobic respiration resumes. Lactate and other intermediates are reutilized or are washed to the systemic circulation. If the period of severe ischemia is extended to 40–60 minutes, the injury becomes irreversible. Such myocytes cannot be salvaged by reperfusion with arterial blood and are necrotic. When reperfused, irreversibly injured myocytes develop contraction-band necrosis and accumulate calcium phosphate. Although unproved, it is possible that some myocytes, alive at the time of reperfusion, may die as a consequence of successful reperfusion. This phenomenon is termed lethal reperfusion injury. Sublethal forms of reperfusion injury, such as stunning, also occur.