Hammond B, Hess M L
J Am Coll Cardiol. 1985 Jul;6(1):215-20. doi: 10.1016/s0735-1097(85)80278-3.
The sequential univalent reduction of oxygen gives rise to very reactive intermediate products including superoxide anion radical, hydrogen peroxide and free hydroxyl radicals. Normally, the tissue concentration of these intermediate products of oxygen is severely limited; however, if oxygen free radicals are produced in excess of the capacity of the tissues to eliminate them, they may cause serious damage. The biochemistry and possible sources of free radical generation in animal models of ischemic/reperfusion injury are reviewed. The ability of scavengers of oxygen free radicals to improve mechanical, mitochondrial and sarcoplasmic reticulum function in animal models of ischemic/reperfusion injury suggests that oxygen free radicals are partly responsible for myocardial injury in these models. Future research should be directed at establishing the relevance of oxygen radical-mediated myocardial injury in the experimental setting to analogous clinical situations.
氧的顺序单价还原产生包括超氧阴离子自由基、过氧化氢和游离羟基自由基在内的非常活泼的中间产物。通常，这些氧中间产物的组织浓度受到严格限制；然而，如果氧自由基的产生超过组织消除它们的能力，它们可能会造成严重损害。本文综述了缺血/再灌注损伤动物模型中自由基产生的生物化学及可能来源。在缺血/再灌注损伤动物模型中，氧自由基清除剂改善机械、线粒体和肌浆网功能的能力表明，氧自由基在这些模型中部分导致心肌损伤。未来的研究应致力于确定实验环境中氧自由基介导的心肌损伤与类似临床情况的相关性。
