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

1.离体大鼠肝线粒体的缺氧孵育引起内膜质子屏障的破坏，随后导致氧化磷酸化的损失。缺氧条件下线粒体功能障碍包括线粒体内ATP耗竭、CaATP^+<2->复合物解离释放游离Ca^+、游离Ca^&lt;2+&gt;激活磷脂酶A_2和破坏内膜质子屏障.胆汁的流速与细胞内ATP水平密切相关。然而，在长时间低温缺氧后，复氧恢复ATP的细胞水平，但不是胆汁排泄率。低温孵育后，肝细胞内大部分代谢酶系统保存完好，如细胞水平的ATP。将离体肝脏置于含Ca^&lt;2+&gt;的培养基中孵育，可对胆汁排泄系统造成严重损害，但不影响细胞内ATP水平。这些数据表明缺血时Ca^&lt;2+&gt;内流导致胆汁形成减少.在大鼠心脏中存在两种形式的ATP，一种可被1H-NMR光谱检测到<31>，另一种则不可检测到。从~ 1HP-NMR的特征<31>看，前者可能是胞浆中的游离ATP，而后者可能是蛋白质结合的和线粒体结合的ATP。在缺血时，胞浆中游离ATP比其它形式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.