陈品珍 成细华 廖菁 陈聪 童巧珍 刘洋 张仪 袁梦

    〔摘要〕 再灌注是急性心肌梗死常用的治疗措施，但再灌注常导致心肌舒缩功能障碍、心肌细胞不可逆损伤加重等并发症，引起心肌缺血再灌注损伤(myocardial ischemia reperfusion injury， MIRI)。胱硫醚-γ-裂解酶(cystathionine-γ-lyase， CSE)/硫化氢(hydrogen sulfide， H2S)通路在MIRI发生发展中起关键保护作用，其机制包括保护线粒体、抗氧化应激、调节内皮一氧化氮合酶活性等多方面，故本文从CSE/H2S产生的调节因素，对MIRI的保护机制及中西医临床应用的最新研究进展作一阐述。

    〔关键词〕 心肌缺血再灌注损伤;CSE/H2S通路;作用机制;H2S供体

    〔中图分类号〕R2;R541? ? ? ?〔文献标志码〕A? ? ? ?〔文章编号〕doi：10.3969/j.issn.1674-070X.2021.01.030

    〔Abstract〕 Reperfusion is a common treatment in acute myocardial infarction. However， reperfusion can cause myocardial systolic and diastolic dysfunction， and aggravate irreversible damage to myocardial cells and other complications， cause myocardial ischemia reperfusion injury (MIRI). The cystathionine-γ-lyase (CSE) / hydrogen sulfide (H2S) pathway plays an important role in the occurrence and development of MIRI， with protective effects including protection of mitochondria， anti-oxidative stress， regulation of endothelial nitric oxide synthase activity. This paper will review the research advances of the regulatory factors for CSE/H2S production ......