Turer Aslan T, Hill Joseph A
Department of Internal Medicine (Cardiology), University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Am J Cardiol. 2010 Aug 1;106(3):360-8. doi: 10.1016/j.amjcard.2010.03.032.
Since the initial description of the phenomenon by Jennings et al 50 years ago, our understanding of the underlying mechanisms of reperfusion injury has grown significantly. Its pathogenesis reflects the confluence of multiple pathways, including ion channels, reactive oxygen species, inflammation, and endothelial dysfunction. The purposes of this review are to examine the current state of understanding of ischemia-reperfusion injury, as well as to highlight recent interventions aimed at this heretofore elusive target. In conclusion, despite its complexity our ongoing efforts to mitigate this form of injury should not be deterred, because nearly 2 million patients annually undergo either spontaneous (in the form of acute myocardial infarction) or iatrogenic (in the context of cardioplegic arrest) ischemia-reperfusion.
自50年前詹宁斯等人首次描述这一现象以来，我们对再灌注损伤潜在机制的理解有了显著进展。其发病机制反映了多种途径的交汇，包括离子通道、活性氧、炎症和内皮功能障碍。本综述的目的是审视目前对缺血再灌注损伤的理解现状，并着重介绍针对这一迄今为止难以捉摸的靶点的最新干预措施。总之，尽管其复杂性高，但我们减轻这种损伤形式的持续努力不应受阻，因为每年有近200万患者经历自发性（以急性心肌梗死形式）或医源性（在心脏停搏情况下）缺血再灌注。
