Department of Anatomy, Medical School, National and Kapodistrian University of Athens, Athens, Greece.
Redox Rep. 2012;17(2):80-3. doi: 10.1179/1351000212Y.0000000002. Epub 2012 Feb 2.
Besides the fact that prolonged whole-body ischemia causes tissue and organ injury during cardiac arrest, additional damage occurs after the restoration of spontaneous circulation, during which the reperfusion activates a host of intracellular responses. These responses may lead to an increased threshold of oxidant-mediated injury and redox-mediated programed cell death in the stunned myocardium. The aim of this article is to summarize the major intracellular responses occurring from the onset of cardiac arrest until the post-resuscitation period that may lead to redox-mediated programed death of myocardial cells.
除了心脏骤停期间长时间全身缺血会导致组织和器官损伤这一事实外，在自主循环恢复后还会发生额外的损伤，在此期间，再灌注会激活一系列细胞内反应。这些反应可能导致心肌顿抑中氧化剂介导的损伤和氧化还原介导的程序性细胞死亡阈值增加。本文的目的是总结从心脏骤停开始到复苏后期间可能导致心肌细胞氧化还原介导程序性死亡的主要细胞内反应。
