Biochemical Process of Ischemic Injury of Liver and Protection against the Injury.

1.大鼠肝线粒体缺氧孵育可破坏内膜质子屏障，从而导致氧化磷酸化的丧失。这种缺氧状态下的线粒体功能障碍包括线粒体内ATP耗竭、CaATP^&lt；2-&gt；复合体解离以释放游离Ca~(2+)、磷脂酶A_2被释放的Ca^&lt；2~+激活以及内膜质子屏障的破坏。胆汁流量与细胞内三磷酸腺苷水平密切相关。然而，在长期低温缺氧后，复氧恢复了细胞内ATP的水平，但不能恢复胆汁排泄率。低温孵育后，肝细胞内的代谢酶系统大部分保存完好，如细胞水平的三磷酸腺苷。离体肝在含Ca~(2+)的培养液中孵育，对胆汁排泄系统造成严重损伤，但不影响细胞内ATP的水平。这些数据表明，缺血时钙离子内流导致胆汁形成减少。在大鼠的心脏中有两种形式的三磷酸腺苷；一种是能被核磁共振波谱检测到的，另一种是不能检测到的。从核磁共振的特征来看，前者似乎是胞浆中的游离ATP，而后者是蛋白质结合的线粒体ATP。在缺血期间，胞浆中的游离ATP似乎比另一种形式的ATP消耗得更快。

1. Anoxic incubation of isolated rat liver mitochondria caused disruption of the proton barrier of the inner membrane which subsequently led to loss of oxidative phosphorylation. This mitochondrial dysfunction under anoxia was involved depletion of intramitochondrial ATP, dissociation of the CaATP^<2-> complex to liberate free Ca^+, activation of phospholipase A_2 by the free Ca^<2+> released and disruption of the proton barrier of the inner membrane.2. The flow rate of bile is closely correlated with the cellular level of ATP. However, after prolonged hypothermic anoxia, reoxygenation restored the cellular level of ATP but not the rate of bile excretion. Most of the metabolic enzyme systems in hepatocytes were well preserved after hypothermic incubation, like the cellular level of ATP. Incubation of isolated liver in medium containing Ca^<2+> caused serious damage to the system for bile excretion without affecting the cellular level of ATP. These data indicated that Ca^<2+> influx during ischemia resulted in decreased bile formation.3. There are two forms of ATP in rat heart; one is detectable by ^<31>P-NMR spectroscopy and the oter is not. From the characteristics of the ^<31>P-NMR, the former seems to be free ATP in the cytosol, and the latter to be protein-bound and mitochondrial ATP. During ischemia, the free ATP in the cytosol seemd to be depleted mopre rapidly than the other form of ATP.