Ischemia, rather than reperfusion, inhibits respiration through cytochrome oxidase in the isolated, perfused rabbit heart: role of cardiolipin
Ischemia, rather than reperfusion, inhibits respiration through cytochrome oxidase in the isolated, perfused rabbit heart: role of cardiolipin
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DOI：
10.1152/ajpheart.00348.2003
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发表时间：
2004-07-01
影响因子：
4.8
通讯作者：
Hoppel, CL
中科院分区：
文献类型：
--
作者：
Lesnefsky, EJ;Chen, Q;Hoppel, CL
缺血和再灌注导致线粒体功能障碍，氧化能力下降，细胞色素c丢失，活性氧产生。在离体灌注兔心脏缺血期间，位于质膜下的肌层下线粒体持续磷脂心磷脂的丢失，通过细胞色素氧化酶和细胞色素c的氧化代谢减少。我们询问在再灌注期间是否会发生涉及心磷脂和细胞色素c和细胞色素氧化酶丢失的远端电子链的额外损伤。再灌注未导致远端电子传递链的额外损伤。细胞色素氧化酶的氧化作用和细胞色素c的含量在再灌注过程中没有进一步降低。因此，心肌磷脂、细胞色素c和细胞色素氧化酶的损伤发生在缺血而不是再灌注期间。缺血损伤导致早期再灌注期氧化功能持续缺陷。心磷脂含量的降低伴随着细胞色素c含量的持续下降和细胞色素氧化酶的氧化，是再灌注过程中心肌细胞额外损伤的潜在机制。
Ischemia and reperfusion result in mitochondrial dysfunction, with decreases in oxidative capacity, loss of cytochrome c, and 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 whether 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.