REACTIVE OXYGEN SPECIES DURING ISCHEMIA REFLOW INJURY IN ISOLATED PERFUSED RAT-LIVER
REACTIVE OXYGEN SPECIES DURING ISCHEMIA REFLOW INJURY IN ISOLATED PERFUSED RAT-LIVER
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DOI：
10.1172/jci113441
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发表时间：
1988-04-01
影响因子：
15.9
通讯作者：
MITCHELL, JR
中科院分区：
文献类型：
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作者：
JAESCHKE, H;SMITH, CV;MITCHELL, JR
在雄性Fischer大鼠的离体灌流肝脏中，验证了肝细胞或网状内皮细胞内产生的活性氧可能导致缺血-再灌注损伤的假说。在灌流液、胆汁和组织中测量GSSG，作为氧化应激的敏感指标。预灌注期30min后，停止灌流(全肝缺血)不同时间(30、120min)，肝脏再灌流60min。胆汁流量(1.48±-)。0.17微升/分钟次数。克肝脏重量)，总谷胱甘肽的胆汁流出量(6.54±-)。0.94nmolGSH eq/min.次。G)和GSSG(1.59.+-.0.23nmolGSH eq/min.次。G)在短期缺血后恢复到69-86%，在缺血2 h后恢复到36-72%，与同期灌流的对照肝脏相比。在再灌流期间，总谷胱甘肽的正弦流出(16.4.+-.2.1nmolGSH eq/min.次。G)和GSSG(0.13.+-.0.05nmolGSH eq/min.次。G)，除了在再灌洗过程中最初的10-30-S升高外，其余均无变化。在再灌流过程中，胆汁中GSSG的分泌在任何时候都可检测到增加。肝脏总谷胱甘肽含量(32.5±-.)3.5nmolGSH eq/mg蛋白)和GSSG(0.27+-)。0.09nmolGSH eq/mg蛋白)在缺血或再灌流的任何时期均无明显变化。因此，我们得出的结论是，在再灌流过程中，最多只有少量的活性氧产生。因此，活性氧不太可能通过脂质过氧化或组织硫醇氧化引起大鼠肝脏的缺血/再灌注损伤。
The hypothesis that intracellular generation of reactive oxygen species in hepatocytes or reticuloendothelial cells may cause ischemia-reperfusion injury was tested in isolated perfused livers of male Fischer rats. GSSG was measured in perfusate, bile, and tissue as a sensitive index of oxidative stress. After a preperfusion phase of 30 min, the perfusion was stopped (global ischemia) for various times (30, 120 min) and the liver was reperfused for another 60 min. The bile flow (1.48 .+-. 0.17 .mu.l/min .times. gram liver weight), the biliary efflux of total glutathione (6.54 .+-. 0.94 nmol GSH eq/min .times. g), and GSSG (1.59 .+-. 0.23 nmol GSH eq/min .times. g) recovered to 69-86% after short-term ischemia and to 36-72% after 2 h of ischemia when compared with values obtained from control livers perfused for the same period of time. During reperfusion, the sinusoidal efflux of total glutathione (16.4 .+-. 2.1 nmol GSH eq/min .times. g) and GSSG (0.13 .+-. 0.05 nmol GSH eq/min .times. g) did not change except for an initial 10-30-s increase during reperfusion washout. No increased GSSG secretion into bile was detectable at any time during reperfusion. The liver content of total glutathione (32.5 .+-. 3.5 nmol GSH eq/mg protein) and GSSG (0.27 .+-. 0.09 nmol GSH eq/mg protein) did not change significantly during any period of ischemia or reperfusion. We conclude, therefore, that at most only a minor amount of reactive oxygen species were generated during reperfusion. Thus, reactive oxygen species are unlikely to cause ischemia/reperfusion injury in rat liver by lipid peroxidation or tissue thiol oxidation.