Complement-Induced Myocardial Ischemia: Neutrophil and Vascular Mechanisms
Medical therapy for acute myocardial infarction is currently directed at preventing acute arrhythmia, limiting the extent of necrosis, and preventing ventricular dilation. Experimental studies dealing with constraining the extent of necrosis in acute coronary occlusion have had limited success in the absence of reperfusion. Restoration of blood flow was found to be by far the most effective mechanism of reducing the degree of necrosis during acute myocardial infarction. Studies in experimental animals indicate that reperfusion within 2–3 h of coronary occlusion in canine hearts results in significant salvage of tissue, defined as the restoration of contractile function to tissue which would have otherwise developed into necrosis. Thus, in the 1980s, attempts to limit injury during acute myocardial infarction are primarily directed at reperfusion. It should be noted, however, that other measures, such as the administration of beta-adrenergic blocking agents, are effective in reducing mortality and perhaps morbidity and should not be neglected.
KeywordsMyocardial Ischemia Leave Anterior Descend Xanthine Oxidase Coronary Blood Flow Arachidonic Acid Metabolism
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