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pubmed:abstractText |
Within minutes of reperfusing ischemic cardiomyocytes, oxidant stress dramatically increases and is associated with postresuscitation injury. Because mitochondria produce deleterious oxidants and useful metabolic substrates, utilization of electron transport chain inhibitors against reperfusion injury, though promising, must not overly compromise recovery of mitochondrial function. This study sought to further characterize the oxidant source at reperfusion and develop a strategy for therapeutic intervention by manipulation of dose, duration, and the degree of reversibility of mitochondrial inhibition.
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pubmed:affiliation |
Emergency Resuscitation Center, Sections of Emergency Medicine, Department of Medicine, University of Chicago, Chicago, Illinois, USA.
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