Reperfusion injury: Experimental evidence and clinical implications
Reperfusion injury: Experimental evidence and clinical implications
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DOI：
10.1016/s0002-8703(99)70323-6
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发表时间：
1999-08-01
影响因子：
4.8
通讯作者：
Tritto, I
中科院分区：
文献类型：
--
作者：
Ambrosio, G;Tritto, I
缺血后再灌注可深刻改变心脏功能。这种现象的主要介质是氧自由基和中性粒细胞。在再流时，大量产生氧自由基，压倒细胞防御并诱导氧化性组织损伤;在缺血后心肌中可以发现氧自由基形成和攻击的生化标记物，缺血后组织中中性粒细胞的再引入伴随着它们的活化，释放直接诱导组织损伤的溶解酶和放大局部炎症反应的促炎介质。中性粒细胞也可能堵塞毛细血管，机械性地阻塞血流。氧化剂还可以调节各种事件，最终导致组织损伤，如一氧化氮形成、血小板活化因子代谢、组织因子合成和粘附分子暴露。在临床环境中，缺血后再灌注的重要后果是可逆性收缩功能障碍（“休克”），其主要由氧自由基攻击引起，以及继发于中性粒细胞堵塞和血管收缩的微血管水平的流动受损（“无复流”）。
Postischemic reperfusion may profoundly alter cardiac function. Principal mediators of this phenomenon are oxygen radicals and neutrophils, Upon reflow, oxygen radicals are generated in large amounts, overwhelming cellular defenses and inducing oxidative tissue damage; biochemical markers of oxygen radical formation and attack can be found in postischemic myocardium, Reintroduction of neutrophils in postischemic tissues is accompanied by their activation, with release of lytic enzymes that directly induce tissue damage and proinflammatory mediators that amplify the local inflammatory reaction. Neutrophils may also plug capillaries, mechanically blocking flow. Oxidants can also modulate various events, ultimately leading to tissue injury, such as nitric oxide formation, platelet-activating Factor metabolism, tissue factor synthesis, and exposure of adhesion molecules. In the clinical setting, important consequences of postischemic reperfusion are reversible contractile dysfunction ("stunning"), which is mostly caused by oxygen radical attack, and impairment to flow at the microvascular level ("no-reflow") secondary to neutrophil plugging and vasoconstriction.