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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。
Objective: To investigate the mechanism of mitochondrial dysfunction induced by biliary obstruction. Methods: The model of biliary obstruction in dogs was replicated. The mitochondrial respiratory function, calcium content, calcium uptake rate, malondialdehyde (MDA) content and the content of superoxide dismutase (SOD) were observed at different time points. Results: The bile duct obstruction in each group (Ⅱ-V group) at 2 weeks, 3 weeks, 4 weeks and 5 weeks was compared with that in sham operation group (Ⅰ): ① The mitochondrial respiratory control rate, calcium uptake rate and SOD content were significantly decreased (P <0.05 in group Ⅱ, P <0.01 in other groups) ② The content of calcium in mitochondria increased significantly (P <0.05 in group Ⅱ, p <0.01 in other groups) ③ The content of MDA in mitochondria increased significantly P <0.01). Correlation analysis showed that the mitochondrial calcium content, MDA content and mitochondrial respiratory control rate showed a significant negative correlation (P <0.01). Conclusion: The mitochondrial respiratory function is obviously damaged after biliary obstruction, and calcium overload and lipid peroxidation may be the possible mechanism of mitochondrial extracorporeal damage.