title: [Pathophysiology of reperfusion].
abstract: We investigated the influence of time after coronary occlusion, of myocardial O2-demand, and of collateral blood flow upon the amount of myocardium that can be salvaged by reperfusion. These studies were carried out in species of mammalian heart that differed widely in the availability of collateral blood flow and in MVO2, i.e. dogs, pigs, cats, rabbits, guinea pigs, and rats. In canines, we increased MVO2 before coronary occlusion by bilateral vagotomy. We found that hearts with measurable collateral blood flow had a markedly increased tolerance toward ischemia and vice versa. Ranking the species from high to low collateral flow (guinea pig, cat, dog, pig, rat) displays the same order when ranked for infarction. In the guinea pig, collateral blood flow was so high that we were unable to produce infarction by coronary ligation. The infarction process was the most rapid in pigs (= 45 min after occlusion) and rats (= 20-45 min after coronary occlusion). Increasing the MVO2 by vagolytic tachycardia markedly decreased the tolerance toward ischemia in the canine heart. We conclude from our experiments that reperfusion is the most powerful intervention to salvage ischemic myocardium, provided it is carried out within the period of reversible ischemic injury. With very low collateral blood flow (as expected to be present in young men with no previous manifestation of ischemic heart disease) this interval of reversibility may be about one hour after coronary occlusion and it is probably shorter in the presence of tachycardia and reduced perfusion pressure.
mesh_terms: D000818:Animals; D003097:Collateral Circulation; D003326:Coronary Circulation; D003327:Coronary Disease / Q000503:physiopathology*; D003328:Coronary Thrombosis / Q000503:physiopathology*; D006439:Hemodynamics; D006801:Humans; D009203:Myocardial Infarction / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism; D010101:Oxygen Consumption; D013610:Tachycardia / Q000503:physiopathology
vernacular_title: Die Pathophysiologie der Reperfusion.