Shibayama Y
Pathol Res Pract. 1987 Jun;182(3):390-5. doi: 10.1016/S0344-0338(87)80075-4.
Pathogenesis of hepatic injury often seen in patients with congestive heart failure is obscure, but hepatic hypoxia and endotoxaemia resulting from congestive heart failure may relate to it. The present study was undertaken in rats to ascertain whether hepatic hypoxia potentiates endotoxin-induced hepatotoxicity. Hypoxic condition of hepatocytes ws induced by exposure to 7% oxygen for 3 hours or administration of ethanol. When endotoxin was given immediately before or several hours after hypoxia, elevation of activities of serum transaminases and focal random hepatocellular necrosis in the lobules were induced, although these functional and morphological changes were not observed in rats with hypoxia or endotoxaemia alone. This finding indicates that hepatic hypoxia leads to a potentiation of sensitivity to endotoxin hepatotoxicity which persists for several hours after recovery from hypoxia. Moreover, these experimental data suggest that hepatic injury in patients with congestive heart failure may be caused by enhancement of endotoxin hepatotoxicity by hepatic hypoxia.
充血性心力衰竭患者中常见的肝损伤发病机制尚不清楚,但充血性心力衰竭导致的肝缺氧和内毒素血症可能与之相关。本研究在大鼠中进行,以确定肝缺氧是否会增强内毒素诱导的肝毒性。通过暴露于7%氧气3小时或给予乙醇来诱导肝细胞的缺氧状态。当在缺氧前或缺氧后数小时立即给予内毒素时,会诱导血清转氨酶活性升高和小叶内局灶性随机肝细胞坏死,尽管在单独存在缺氧或内毒素血症的大鼠中未观察到这些功能和形态学变化。这一发现表明,肝缺氧会导致对内毒素肝毒性的敏感性增强,这种增强在缺氧恢复后可持续数小时。此外,这些实验数据表明,充血性心力衰竭患者的肝损伤可能是由肝缺氧增强内毒素肝毒性所致。