Suzuki K, Koyama K, Asanuma Y, Ouchi S, Tanaka J, Shirayama K, Yoshida S
Department of Surgery, Akita University School of Medicine, Japan.
Nihon Geka Gakkai Zasshi. 1988 May;89(5):703-8.
Obstructive jaundice model was created using rats by the ligation of bile duct. One, 2, 3 weeks later, the respiratory function and morphology of the hepatic mitochondria were comparatively evaluated between mitochondria directly fractionated from liver tissue and mitochondria from isolated hepatocytes. Respiratory function of the former deteriorated with the duration of jaundice. ATP synthesis decreased to 75% of the control at 1 and 2 weeks, and 58% at 3 weeks after ligation. On the contrary, it was 97%, 88% and 87% of the control. On the contrary, it was 97%, 88% and 87% of the control at 1, 2 and 3 weeks in the latter. By electron microscopic examination, the size of mitochondria of the jaundiced liver is inconsistent and smaller in general than the control. These data suggest that the deterioration of mitochondrial function in the jaundiced liver is not caused mainly by the disturbance of mitochondria themselves, but caused by the respiratory inhibitory factors which exist around the mitochondria.
通过结扎胆管的方式利用大鼠建立梗阻性黄疸模型。在结扎后的1周、2周、3周，对直接从肝组织分离得到的线粒体与从分离的肝细胞中得到的线粒体的呼吸功能和肝线粒体形态进行了比较评估。前者的呼吸功能随黄疸持续时间而恶化。结扎后1周和2周时，ATP合成降至对照组的75%，3周时降至58%。相反，后者在1周、2周和3周时分别为对照组的97%、88%和87%。通过电子显微镜检查，黄疸肝中线粒体的大小不一致，总体上比对照组小。这些数据表明，黄疸肝中线粒体功能的恶化并非主要由线粒体自身的紊乱引起，而是由线粒体周围存在的呼吸抑制因子所致。
