Studies of experimental coronary artery reperfusion. Effects on infarct size, myocardial function, biochemistry, ultrastructure and microvascular damage.
The present report is a review of recent experimental studies in a canine model of acute coronary occlusion. The questions addressed were: (1) Does coronary reperfusion reduce myocardial infarct size? (2) What is the relationship between microvascular damage and hemorrhage and the development of myocardial necrosis? (3) What are the biochemical, functional and ultrastructural characteristics of reperfused tissue salvaged from necrosis? Coronary occlusion followed by reperfusion in the dog resulted in significant subepicardial salvage of myocardium if reperfusion was instituted before 6 hours of ischemia. Because ultrastructural evidence of microvascular damage was found only after irreversible damage to myocytes, and because gross hemorrhage after coronary reperfusion was confined to zones of myocardium that were already necrotic, it does not appear that hemorrhage should serve as a deterrent to reperfusing reversibly injured myocytes. Severely ischemic myocardium that had been salvaged by coronary reperfusion required several days before it returned to normal from biochemical, functional and ultrastructural standpoints.
D000255:Adenosine Triphosphate / Q000032:analysis; D000818:Animals; D009202:Cardiomyopathies / Q000473:pathology; D003326:Coronary Circulation; D004285:Dogs; D006321:Heart / Q000503:physiopathology; D006470:Hemorrhage / Q000473:pathology; D006801:Humans; D008833:Microcirculation / Q000473:pathology; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D009206:Myocardium / Q000032:analysis / Q000648:ultrastructure; D010725:Phosphocreatine / Q000032:analysis
D010725:Phosphocreatine; D000255:Adenosine Triphosphate