[From ischemia to reperfusion lesions].
It is well established that early reperfusion of ischemic myocardium limits or even prevents necrosis. However, sometimes restitution of coronary flow to the ischemic myocardium may precipitate a sequence of events that would have occurred either later or not at all. To prove the existence of reperfusion-induced injury, it is necessary to show that cells, potentially viable before reperfusion, are killed by the onset of reperfusion. The consequences of reperfusion are reperfusion-induced arrhythmias, myocardial stunning, accelerated necrosis and lethal reperfusion injury. The two main theories explaining the development of reperfusion injury are formation of free radicals and cellular calcium overload. Free radicals produced during early reperfusion may cause oxidant stress to membrane lipids and proteins associated with a potassium loss and a temporary cytosolic calcium overload. Results of experiments with free radical scavengers are contradictory for unknown reasons suggesting that reperfusion injury is a complex event innowing endothelial damage, leukocyte-plugged vessels, microvascular damage and production of heat-shock proteins.
Rochette
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Facultés de médecine et de pharmacie, Laboratoire de physiopathologie et pharmacologie cardiovasculaires expérimentales, Dijon.
Maupoil
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D001145:Arrhythmias, Cardiac / Q000503:physiopathology; D000242:Cyclic AMP / Q000032:analysis; D005609:Free Radicals; D006801:Humans; D017202:Myocardial Ischemia / Q000503:physiopathology* / Q000628:therapy; D015425:Myocardial Reperfusion; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology*; D013564:Sympathetic Nervous System / Q000503:physiopathology
D005609:Free Radicals; D000242:Cyclic AMP
De l'ischémie aux lésions de reperfusion.