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本文介绍心肌缺血再灌注补体激活，过敏毒素和膜攻击复合物的形成以及它们通过不同途径对靶细胞所发挥的生物学效应。同时就血管紧张素转换酶抑制卡托普利抗补体介导的心肌缺血再灌注损伤的作用的可能机制作了阐述。
This article describes the role of complement activation, the formation of anaphylatoxins and membrane attack complexes in myocardial ischemia-reperfusion, and their biological effects on target cells through different pathways. At the same time, angiotensin-converting enzyme inhibits the possible mechanism of captopril anti-complement-mediated myocardial ischemia-reperfusion injury.