Lesnefsky Edward J, Chen Qun, Slabe Thomas J, Stoll Maria S K, Minkler Paul E, Hassan Medhat O, Tandler Bernard, Hoppel Charles L
Division of Cardiology, Department of Medicine, School of Dental Medicine, Case Western Reserve University, Cleveland, OH 44106, USA.
Am J Physiol Heart Circ Physiol. 2004 Jul;287(1):H258-67. doi: 10.1152/ajpheart.00348.2003. Epub 2004 Feb 26.
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.
缺血和再灌注会导致线粒体功能障碍，表现为氧化能力下降、细胞色素c丢失以及活性氧的产生。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心磷脂的丢失，通过细胞色素氧化酶的氧化代谢减少以及细胞色素c的丢失。我们研究了在再灌注期间，涉及心磷脂的远端电子链是否会因细胞色素c和细胞色素氧化酶的丢失而受到额外损伤。再灌注并未导致远端电子传递链的额外损伤。在再灌注期间，通过细胞色素氧化酶的氧化以及细胞色素c的含量并未进一步降低。因此，心磷脂、细胞色素c和细胞色素氧化酶的损伤发生在缺血期间而非再灌注期间。缺血性损伤导致再灌注早期氧化功能持续存在缺陷。心磷脂含量的降低伴随着细胞色素c含量的持续下降以及通过细胞色素氧化酶的氧化减少，这是再灌注期间心肌细胞额外损伤的潜在机制。
