心肌缺血再灌注损伤机制研究的回顾与展望

Review and prospect on the mechanism of myocardial ischemia-reperfusion injury

心肌梗死是全球冠心病患者死亡的主要原因之一。在急性心肌梗死早期行经皮冠状动脉介入术、冠状动脉旁路移植术、药物等治疗手段,可恢复缺血区心肌组织血供,挽救濒死的心肌,降低患者的致死率。然而,心肌血供中断后,一定时间内再通恢复血供后,原缺血心肌可发生较缺血时更为严重的损伤,这一现象称为心肌缺血再灌注损伤(MIRI),其发生机制尚未完全阐明。文章就近年来MIRI机制的研究进展作一综述,阐述MIRI的病理生理机制,将有助于开发新的治疗干预手段,为临床治疗心肌梗死提供帮助。

Myocardial infarction is one of the leading causes of death in patients with coronary heart disease worldwide. In the early stage of acute myocardial infarction, percutaneous coronary intervention, coronary artery bypass grafting, drugs and other treatment means can restore the blood supply of ischemic myocardial tissue, save the dying myocardium and reduce the mortality rate of patients. However, after the interruption of myocardial blood supply and the restoration of blood supply within a certain period of time, the original ischemic myocardium may suffer more serious damage than that of ischemia. This phenomenon is called myocardial ischemia-reperfusion injury(MIRI), and its mechanism has not been fully elucidated. In this paper, the research progress of MIRI mechanism in recent years is reviewed, and the pathophysiological mechanism of MIRI is expounded, which will help to develop new therapeutic interventions and provide help for clinical treatment of myocardial infarction.