Watanabe H, Onda M, Genga A, Asano G
First Department of Surgery, Nippon Medical School, Tokyo, Japan.
Nihon Geka Gakkai Zasshi. 1993 Dec;94(12):1269-76.
The effects of ischemia and reperfusion with and without oxygen radical scavengers and xanthine oxidase inhibitors on Ca(2+)-ATPase activity were examined in the rat liver of 5 min ischemia followed by 5 and 10 min reperfusion. Ischemia was produced by the ligation of right hepatic artery and right portal vein. Superoxide dismutase, catalase and allopurinol were administered by subcutaneous injection of 60,000U/kg, 90,000U/kg and 200mg/kg, respectively before ligation. Reaction products of Ca(2+)-ATPase were morphometrically analyzed by RUZEX IIIU. Histochemically, Ca(2+)-ATPase activities were demonstrated on plasma membrane of liver cells, bile canaliculi and Kupffer cells involving mitochondria in liver cells of control rats. Ca(2+)-ATPase activities were depressed in the central lobes of liver after 5 min ischemia followed by 5 and 10min reperfusion. However, the activities of Ca(2+)-ATPase were not depressed by addition of oxygen radical scavengers and xanthine oxidase inhibitor before ischemia. These results suggest that oxygen free radicals may influence Ca(2+)-ATPase activity and contribute to liver cell damage due to ischemia-reperfusion.
在大鼠肝脏中，结扎右肝动脉和右门静脉造成5分钟缺血，然后分别再灌注5分钟和10分钟，研究有无氧自由基清除剂和黄嘌呤氧化酶抑制剂时缺血再灌注对Ca(2+)-ATP酶活性的影响。在结扎前分别皮下注射超氧化物歧化酶60,000U/kg、过氧化氢酶90,000U/kg和别嘌呤醇200mg/kg。用RUZEX IIIU对Ca(2+)-ATP酶的反应产物进行形态计量分析。组织化学显示，在对照大鼠肝细胞的质膜、胆小管和包括线粒体在内的库普弗细胞上有Ca(2+)-ATP酶活性。缺血5分钟后再灌注5分钟和10分钟，肝脏中央叶的Ca(2+)-ATP酶活性降低。然而，在缺血前添加氧自由基清除剂和黄嘌呤氧化酶抑制剂不会使Ca(2+)-ATP酶活性降低。这些结果表明，氧自由基可能影响Ca(2+)-ATP酶活性，并导致缺血再灌注引起的肝细胞损伤。
