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目的探讨继发性胆汁性肝硬化时肝线粒体呼吸功能及呼吸酶的损伤及其机制。方法双重结扎犬胆总管5周复制继发性胆汁性肝硬化模型，用差速离心法分离肝线粒体，观察肝线粒体呼吸功能，线粒体院琥珀酸脱氢酶（SDH）、细胞色素C氧化酶（CCO）活力及线粒体Ca2+、丙二醛（MDA）、超氧化物歧化酶（SOD）含量变化。结果继发性胆汁性肝硬化时肝线粒体呼吸功能、呼吸酶SDH及CCO活力均显著降低，线粒体Ca2+及MDA含量明显升高，SOD含量则显著下降。结论继发性胆汁性肝硬化时肝线粒体呼吸功能及呼吸酶系受到明显损伤，钙超载及脂质过氧化反应是造成线粒体损伤的重要原因。
Objective To investigate the mitochondrial respiratory function and respiratory enzyme damage and its mechanism in secondary biliary cirrhosis. Methods The model of secondary biliary cirrhosis was established by double ligation of the common bovine common bile duct. The mitochondria were isolated by differential centrifugation. The mitochondrial respiratory function, mitochondrial succinate dehydrogenase (SDH) and cytochrome C oxidase CCO) and the content of Ca2 +, malondialdehyde (MDA) and superoxide dismutase (SOD) in mitochondria. Results Respiratory function, respiration enzyme SDH and CCO of liver mitochondria decreased significantly in secondary biliary cirrhosis. The content of Ca2 + and MDA in mitochondria increased significantly and the content of SOD decreased significantly. Conclusions Secondary mitochondrial respiratory function and respiratory enzymes are significantly damaged in secondary biliary cirrhosis. Calcium overload and lipid peroxidation are the important causes of mitochondrial damage.