Itoh H, Miyazaki M, Udagawa I, Koshikawa H, Okui K
First Department of Surgery, Chiba University, School of Medicine.
Nihon Shokakibyo Gakkai Zasshi. 1991 May;88(5):1200-7.
The hepatic cellular damage induced by liver ischemia was investigated in rats with obstructive jaundice. Hepatic tissue blood flow in obstructive jaundice was decreased in the relation to the duration of jaundice. The value of lipid peroxide and cathepsin D activity of the hepatic tissue increased in the obstructive jaundice. Therefore, it was suggested that cell membrane and lysosomal membrane injury were induced in obstructive jaundice. The value of lipid peroxide of hepatic tissue in obstructive jaundice was more increased after partial liver ischemia. The survival rate following hepatic ischemia in jaundiced rats was remarkably lower than that of normal rats, and also it related to the duration of jaundice. In addition, histological changes of the liver after partial ischemia are severe in obstructive jaundiced liver. These data suggest that more remarkable hepatic cellular damage than in normal liver may be induced by liver ischemia in obstructive jaundice.
在阻塞性黄疸大鼠中研究了肝脏缺血诱导的肝细胞损伤。阻塞性黄疸时肝脏组织血流随黄疸持续时间的延长而减少。阻塞性黄疸时肝组织中脂质过氧化物值和组织蛋白酶D活性增加。因此，提示阻塞性黄疸可诱导细胞膜和溶酶体膜损伤。部分肝脏缺血后，阻塞性黄疸肝组织中脂质过氧化物值进一步升高。黄疸大鼠肝脏缺血后的存活率显著低于正常大鼠，且与黄疸持续时间有关。此外，部分缺血后阻塞性黄疸肝脏的组织学变化更为严重。这些数据表明，阻塞性黄疸时肝脏缺血可能比正常肝脏诱导更显著的肝细胞损伤。
