Role of the hepatovasculature in free radical mediated reperfusion damage of the liver.

摘要: This study was undertaken in order to assess the role of purely circulation-related effects upon free-radical-mediated reperfusion injury liver by comparing respective oxygen free-radical scavenger superoxide dismutase (SOD) and vasodilative action papaverine an ischemia/reperfusion model liver. Livers from male Wistar rats were rinsed blood free via portal vein stored ischemically (60 min at 37 °C Krebs-Henseleit solution 60 4 Euro-Collins solution). Reperfusion carried out a constant flow 30 ml/min for 45 nonrecirculating manner. Warm ischemic damage evident untreated livers compared control livers, submitted solely cold ischemia 2 h 4°C, increased vascular resistance reperfusion, enhanced enzyme leakage parenchyme (glutamate pyruvate transaminase, glutamate dehydrogenase) endothelium (purine-nucleoside phosphorylase), reduced tissue content ATP lipid peroxidation. Preischemic treatment with SOD or (the latter also given during reperfusion) significantly hepatic parenchymal loss comparable Both drugs resulted significant increase end reperfusion. SOD, but not papaverine, prevented purine-nucleoside phosphorylase levels peroxides. Since induced vasodilatation mimicked beneficial on hepatocellular viability after we conclude that toxic species exert major impact system hepatocyte is altered circulatory disturbances which can be as well papaverine.