活性氧在急性心肌梗死心肌再灌注损伤中的作用和机制

The effect and mechanism of reactive oxygen species on myocardial ischemia reperfusion injury in acute myocardial infarction

缺血再灌注(ischemia reperfusion,IR)损伤是急性心肌梗死(acute myocardial infarction,AMI)重要的病理机制,是组织对缺血后血液灌注恢复的固有反应,增加了AMI的病死率和并发症。这是一个复杂的过程,包括在细胞内和细胞外环境中发生的多种机制,在这个过程中大部分机制是由活性氧(reactive oxygen species,ROS)介导的。对于IR损伤,寻找一个心脏保护剂和抗氧化剂来调节ROS浓度,进行预处理,对改善心脏功能和延缓心肌坏死具有非常重要的临床意义。本文就ROS在AMI再灌注损伤中的机制及信号靶点予以阐述,为临床防治心肌梗死再灌注损伤提供新的思路和方法。

Ischemia reperfusion（IR）is an important pathomechanism of acute myocardial infarction（AMI）,which is an inherent response to the restoration of blood flow after ischemia.IR-induced tissue injuries contribute to morbidity and mortality in AMI.It is a complex process involving numerous mechanisms occurring in the intracellular and extracellular environments,and it is mediated in part by reactive oxygen species（ROS）.It is of great clinical importance to generate cardioprotective agents and antioxidants to adjust the concentration of ROS,resulting in the development of proper preconditioning,improvement of organ function,delay of the onset of necrosis,In this paper,the mechanism and signal targets of ROS in the perfusion injury of myocardial infarction are reviewed,and the clinical significance of the refilling injury of myocardial infarction is very important.