首页> 外文期刊>American Journal of Physiology >Ischemia, rather than reperfusion, inhibits respiration through cytochrome oxidase in the isolated, perfused rabbit heart: role of cardiolipin.
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Ischemia, rather than reperfusion, inhibits respiration through cytochrome oxidase in the isolated, perfused rabbit heart: role of cardiolipin.

机译:缺血而不是再灌注,通过离体的灌注兔心脏中的细胞色素氧化酶抑制呼吸作用:心磷脂的作用。

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摘要

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.
机译:缺血和再灌注导致线粒体功能障碍,氧化能力降低,细胞色素c损失和活性氧种类的产生。在离体灌注兔心脏缺血期间,位于质膜下方的肌膜下线粒体维持磷脂质心磷脂的丢失,并通过细胞色素氧化酶的氧化代谢减少和细胞色素c的丢失。我们询问在再灌注过程中是否发生涉及心磷脂的远端电子链进一步损伤,并伴有细胞色素c和细胞色素氧化酶的损失。再灌注并没有导致远端电子传输链的额外损伤。在再灌注期间,通过细胞色素氧化酶的氧化和细胞色素c的含量没有进一步降低。因此,对心磷脂,细胞色素c和细胞色素氧化酶的损伤发生在局部缺血而非再灌注期间。在早期的再灌注期间,缺血性损伤导致氧化功能的持续缺陷。心磷脂含量的降低,伴随着细胞色素c含量的持续减少和通过细胞色素氧化酶的氧化,是再灌注过程中额外的心肌细胞损伤的潜在机制。

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