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1 Department of Medicine (Division of Cardiology), Case Western Reserve University School of Medicine, Cleveland, OH, USA; Department of Medical, Case Western Reserve University, Cleveland, OH, USA
2 Department of Medicine (Division of Cardiology), Case Western Reserve University School of Medicine, Cleveland, OH, USA
3 Department of Medical, Case Western Reserve University, Cleveland, OH, USA
4 Departmetn of Laboratory Medicine, Case Western Universtiy, Cleveland, OH, USA
5 Medicine (Division of Clinical Pharmacology), Case Western Reserve University School of Medicine, Cleveland, OH, USA; Department of Pharmacology, Case Western Reserve University School of Medicine, Cleveland, OH, USA; Department of Medical, Case Western Reserve University, Cleveland, OH, USA
* To whom correspondence should be addressed. E-mail: EXL9{at}po.cwru.edu.
Ischemia and reperfusion result in mitochondrial dysfunction with decreases in oxidative capacity, loss of cytochrome c, and the generation of reactive oxygen species. During ischemia of the isolated perfused rabbit heart, subsarcolemmal mitochondria, located beneath the plasma membrane, sustain a loss of the phospholipid cardiolipin, with decreases in oxidative metabolism through cytochrome oxidase and the loss of cytochrome c. We asked if additional injury to the distal electron chain involving cardiolipin with loss of cytochrome c and cytochrome oxidase occurs during reperfusion. Reperfusion did not lead to additional damage in the distal electron transport chain. Oxidation through cytochrome oxidase and the content of cytochrome c did not further decrease during reperfusion. Thus, injury to cardiolipin, cytochrome c, and cytochrome oxidase occurs during ischemia, rather than during reperfusion. The ischemic injury leads to persistent defects in oxidative function during the early reperfusion period. The decrease in cardiolipin content accompanied by persistent decrements in the content of cytochrome c and oxidation through cytochrome oxidase is a potential mechanism of additional myocyte injury during reperfusion.
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