肝动脉缺血对供肝细胞的损伤机理及防护措施:Ⅲ.线粒体功能损伤的酶学变化

通过建立16例“简易犬自体肝原位移植模型”，用酶组化光镜观察及分离肝细胞酶活性定量测定技术，检测了肝组织细胞在肝动脉系统缺血（HAI）1h及3h的情况下其SDH（琥珀酸脱氢酶）和LDH（乳酶脱氢酶）的活性，并与正常肝细胞及冷缺血15min的肝细胞作了比较。结果显示：当HAI达1h，肝细胞线粒体SDH活性已明显减低，而LDH活性显著增高，与冷缺血15min组对照有显著性差异（P＜0．001）；当HAI达3h时SDH活性极度减低，而LDH活性极度亢进。提示：HAI可能是移植术后供肝病变致某些早期并发症和胆道并发症的重要因素之一，应尽量限制在1h以内。

STUDY OF THE MECHANISM OF DONOR'S HEPATIC CELLULAR INJURY DUE TO HEPATIC ARTERY ISCHEMIA AND THE PROTECTIVE MEASURES:Ⅲ. ENZYMATIC CHANGES OF MITOCHONDRIAL FUNCTIONAL IMPAIRMENT

On the basis of setting up sixteen simple canine models of orthotopic auto-transplantation of the liver, using LM observation on enzymic histochemical changes and the technique of quantitative assay of enzymatic activity of isolated liver cell,the SDH and LDH activities of hepatic cells were assayed 1h and 3h after hepatic artery ischemia respectively. The results were compared with those of normal hepatic cells and the hepatic cells treated by cold ischemia for 15 min. The results showed: HAI for 1h, the SDH activity of mitochondria of hepatic cells decreased and LDH activity increased obviously. These is a significant difference when compared with cold ischemia for 15min (P＜0. 001) ; when HAI being for 3h, SDH activity decreased and LDH activity increased extremely. The above results imply that HAI is one of the important factors which result in pathological changes of donor's liver cells leading to early stage complications and biliary complications after liver transplantation. The ischemiatime ought to be limited within 1h.