Koyama K, Ito K, Ouchi K, Sato T
Tohoku J Exp Med. 1980 May;131(1):59-69. doi: 10.1620/tjem.131.59.
An investigation was performed of the liver mitochondrial respiratory function in rats after 1, 3 and 6 weeks of biliary obstruction and the following results were obtained: 1) Various parameters of liver mitochondrial respiratory function, such as respiratory control ratio, ADP/O, O2 consumption in state 3 respiration and adenosine triphosphate synthesis were found to decrease with prolongation of biliary obstruction. 2) The mitochondrial respiratory enzymes, cytochrome a (+a3) and cytochrome c(+c1) showed that both decreased in contents with prolongation of obstruction, particularly the latter. 3) The activation ratio of ATPase (latent ATPase/dinitrophenol stimulated ATPase) was increased after long term biliary obstruction, which was thought to indicate the severe damage of mitochondrial membrane. 4) Investigation of the respiratory function with the various respiratory substrates showed that the locations of mitochondrial respiratory inhibition in obstructive jaundice are at sites 1 and 2, which is the same as the situation seen in nonspecific damage of mitochondria. 5) There was a high degree of mitochondrial respiratory disturbance by bile acids, particularly CDCA, which is thought to be one of the causal factors of liver dysfunction in obstructive jaundice. 6) Mitochondrial respiratory function was markedly disturbed in hypotension, and the degree of which correlated with length of time of biliary obstruction.
对胆管阻塞1周、3周和6周后的大鼠肝脏线粒体呼吸功能进行了研究，结果如下：1）随着胆管阻塞时间的延长，肝脏线粒体呼吸功能的各项参数，如呼吸控制率、ADP/O、状态3呼吸中的氧气消耗和三磷酸腺苷合成均降低。2）线粒体呼吸酶细胞色素a（+a3）和细胞色素c（+c1）的含量均随着阻塞时间的延长而降低，尤其是后者。3）长期胆管阻塞后，ATP酶的激活率（潜在ATP酶/二硝基苯酚刺激的ATP酶）升高，这被认为表明线粒体膜受到严重损伤。4）用各种呼吸底物进行呼吸功能研究表明，梗阻性黄疸中线粒体呼吸抑制的部位在部位1和部位2，这与线粒体非特异性损伤的情况相同。5）胆汁酸，尤其是鹅去氧胆酸，对线粒体呼吸有高度干扰，这被认为是梗阻性黄疸肝功能障碍的病因之一。6）低血压时线粒体呼吸功能明显紊乱，其程度与胆管阻塞时间相关。
