Carden D L, Korthuis R J
Department of Physiology, LSU Medical Center, School of Medicine, Shreveport, LA 71130.
Microcirc Endothelium Lymphatics. 1989 Jun-Oct;5(3-5):277-98.
In 1981, it was first proposed that xanthine oxidase-derived reactive oxygen metabolites contribute to the microvascular and parenchymal cell damage which occurs when ischemic tissues are reperfused. Figure 1 summarizes a scheme that has been proposed to explain the interaction of xanthine oxidase-derived oxidants, neutrophil infiltration, and the microvascular dysfunction which occurs in postischemic tissue. According to this proposal, xanthine oxidase-derived oxidants, produced at the time of reperfusion, initiate the formation and release of proinflammatory agents, which subsequently attract and activate neutrophils. The activated granulocytes adhere to vascular endothelium, extravasate, and release cytotoxic oxidants and/or non-oxidative toxins (e.g. proteases) which contribute to tissue destruction. The objective of this review is to summarize the supportive evidence for this scheme in postischemic skeletal muscle and to identify the components of the mechanism that may be amenable to pharmacologic intervention.
1981年，首次有人提出黄嘌呤氧化酶衍生的活性氧代谢产物会导致缺血组织再灌注时发生的微血管和实质细胞损伤。图1总结了一个已被提出的用以解释黄嘌呤氧化酶衍生的氧化剂、中性粒细胞浸润以及缺血后组织中发生的微血管功能障碍之间相互作用的方案。根据这一方案，再灌注时产生的黄嘌呤氧化酶衍生的氧化剂会引发促炎因子的形成和释放，这些促炎因子随后会吸引并激活中性粒细胞。被激活的粒细胞黏附于血管内皮，渗出并释放细胞毒性氧化剂和/或非氧化性毒素（如蛋白酶），这些物质会导致组织破坏。这篇综述的目的是总结在缺血后骨骼肌中支持该方案的证据，并确定该机制中可能适合药物干预的组成部分。
