Mechanisms of postischemic vascular dysfunction in skeletal muscle: implications for therapeutic intervention.

D L Carden, R J Korthuis
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Abstract

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.

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骨骼肌缺血后血管功能障碍的机制:治疗干预的意义。
1981年,首次提出黄嘌呤氧化酶衍生的活性氧代谢物有助于缺血组织再灌注时微血管和实质细胞的损伤。图1总结了一种已经提出的方案,用于解释黄嘌呤氧化酶衍生的氧化剂、中性粒细胞浸润和缺血后组织中发生的微血管功能障碍之间的相互作用。根据这一建议,在再灌注时产生的黄嘌呤氧化酶衍生的氧化剂启动促炎剂的形成和释放,促炎剂随后吸引和激活中性粒细胞。活化的粒细胞粘附在血管内皮外渗,并释放细胞毒性氧化剂和/或非氧化性毒素(如蛋白酶),导致组织破坏。本综述的目的是总结这一方案在缺血性骨骼肌中的支持证据,并确定可能适用于药物干预的机制的组成部分。
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