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缺血再灌注损伤在心、脑、肝、肾等器官均有表现。由于内皮细胞（ＥＣ）所处的特殊解剖位置及生理特点，对钙稳态、血凝稳定以及缺血再灌注稳态等的维持都有重要作用。ＥＣ不仅是缺血再灌注损伤的靶器官，而且是氧自由基产生的主要部位，同时又具有抗氧化作用。在体、离体器官缺血再灌损伤模型以及缺氧处理分离培养的ＥＣ研究均表明：缺血再灌可引起ＥＣ代谢、功能的改变，进而引起ＥＣ损伤甚至死亡。本文从活性氧的产生、高钙负荷、炎性介质、细胞粘附等方面阐述血管ＥＣ在缺血再灌注损伤中的发病意义
Ischemia-reperfusion injury in the heart, brain, liver, kidney and other organs have performance. Due to the special anatomic location and physiological characteristics of endothelial cells (ECs), they play an important role in the maintenance of calcium homeostasis, stabilization of blood clotting and maintenance of ischemia-reperfusion homeostasis. EC is not only the target organ of ischemia-reperfusion injury, but also the main part of oxygen free radical production, and at the same time it has anti-oxidant effect. In vivo, isolated organ ischemia-reperfusion injury model and EC study of hypoxia treatment showed that: ischemia-reperfusion can cause changes in EC metabolism, function, and then cause EC damage and even death. This article elaborates the significance of vascular EC in the pathogenesis of ischemia-reperfusion injury from the aspects of active oxygen production, high calcium load, inflammatory mediators and cell adhesion