摘要
目的：初步探讨胆道梗阻对肝线粒体功能损伤的机制。方法：复制犬胆道梗阻模型，观察梗阻的不同时段肝线粒体呼吸功能、钙含量、钙摄取率、丙二醛（MDA）含量及超氧化物歧化酶（SOD）含量的变化。结果：胆道梗阻2周、3周、4周及5周各组（Ⅱ－V组）分别与假手术组（Ⅰ组）比较：①肝线粒体呼吸控制率、钙摄取率及SOD含量均明显下降（Ⅱ组P＜0.05，其余组P＜0．01）②线粒体钙含量均明显升高（Ⅱ组P＜0．05，其余组p＜0．01）③线粒体MDA含量明显升高（各组P＜0.01）。相关分析显示，线粒体钙含量、MDA含量与线粒体呼吸控制率变化之间均呈现显著的负相关（P＜0．01）。结论：胆道梗阻后肝线粒体呼吸功能受到明显损伤，钙超载及脂质过氧化反应是造成线粒体外能损害的可能机制。
Preliminary studies on the mechanisnl of liver mitochondrial function injury following biliary obstruction.METHODS: The changes of hepatic mitochondrial respiratory respiratory function,calcium content,calcium uptake,malondialdehye(MDA) content and superoxide dismuthe(SOD) content following biliap obstruction in dogs were observed RESULTS: Each grouop of 2, 3, 4, 5 weeks following biliary obstnJction were compatal with sham groupl the results showed:hepatic mitochondrial respiratory control rate (RCR), Ca2+ - uptake and SOD content were reduced significantly (2weeks group P< 0. 05, other groups P < 0. 01 ); hepatic mitochondrial Ca2+ content was incnd significantly (2 weeksgrouP P < 0. 05, other groups P < 0. 01 ); hepatic mitochondrial MDA content were increased significantly (P < 0. 01 ).Mithehondrial calcium conent and MDA content were highly negahve correlated with mitochondnal RCR(P < 0. 01 ). CON'CLUSION:The hepatic mitochondrial respiratory function is obviously damaged after biliary obstiuchoin. Mitochondrial cal-cium overload and lipid peroaldation may be the mechanisms of mitochondroal dysfunction
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1999年第10期909-911,共3页
Chinese Journal of Pathophysiology
关键词
线粒体
脂质过氧化
胆道梗阻
肝功能
Cholestasis
Mitochondria, liver
Calcium
Lipid peroxidation
