Brass C A, Nunes F, Nagpal R
Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia.
Transplantation. 1994 Dec 27;58(12):1329-35.
Despite general agreement on the importance of oxyradicals in mediating "reperfusion" injury, the precise event(s) mediated by increased free radical production remain unclear. In this study we describe for the first time a model of unenhanced chemiluminescence of isolated perfused rat liver demonstrating a marked increase in oxyradical production after reoxygenation. Using aspartate aminotransferase and purine nucleoside phosphorylase release as measures of liver injury, there was no direct link between oxyradical production and hepatic injury. However, there was an abrupt increase in neutrophil chemotaxis activity in the perfusate at the time of reoxygenation with a subsequent decrement, following the pattern of oxyradical production. These data suggest that free radical formation during hepatic reperfusion may mediate signal transduction, as opposed to direct cell injury, as a primary mechanism of action.
尽管对于氧自由基在介导“再灌注”损伤中的重要性已达成普遍共识，但自由基产生增加所介导的确切事件仍不清楚。在本研究中，我们首次描述了一种分离的灌注大鼠肝脏的非增强化学发光模型，该模型显示复氧后氧自由基产生显著增加。使用天冬氨酸转氨酶和嘌呤核苷磷酸化酶的释放作为肝损伤的指标，氧自由基产生与肝损伤之间没有直接联系。然而，在复氧时灌注液中的中性粒细胞趋化活性突然增加，随后下降，呈现出与氧自由基产生相同的模式。这些数据表明，肝再灌注期间自由基的形成可能介导信号转导，而非直接细胞损伤，这是其主要作用机制。
