Israel Y, Orrego H
Clin Gastroenterol. 1981 May;10(2):355-73.
In conclusion, the studies presented suggest that two factors commonly occurring in the alcoholic, namely, an increased rate of ethanol metabolism and hepatomegaly, may have important pathogenic implications in alcoholic liver disease. An increased rate of ethanol metabolism is linked to a greater oxygen demand, thus resulting in greater susceptibility to hypoxia in Zone 3 of the liver acinus, a factor which might be responsible for hepatocellular necrosis in alcoholic hepatitis. Propylthiouracil has been shown to have a protective effect against hypoxic necrosis in alcohol-fed animals and has been found to be most effective in accelerating the rate of recovery of alcoholics with active liver disease. On the other hand, hepatocyte expansion in hepatomegaly, in the face of a semi-rigid liver capsule, leads to constriction of extracellular volume and to an increase in intrahepatic and portal pressure. The latter, in turn, could produce a variety of haemodynamic alterations as those found in the alcoholic. To what extent the mechanisms described are responsible for or might add to the myriad of other disturbances observed in alcoholic disease should be further analysed.
总之，所呈现的研究表明，酒精中毒者中常见的两个因素，即乙醇代谢率增加和肝肿大，可能在酒精性肝病中具有重要的致病意义。乙醇代谢率增加与更大的氧气需求相关，从而导致肝腺泡3区对缺氧的易感性增加，这一因素可能是酒精性肝炎肝细胞坏死的原因。已证明丙硫氧嘧啶对酒精喂养动物的缺氧坏死具有保护作用，并且发现它在加速患有活动性肝病的酒精中毒者的恢复速度方面最为有效。另一方面，在肝肿大的情况下，面对半刚性的肝包膜，肝细胞扩张会导致细胞外液体积缩小以及肝内和门静脉压力升高。后者继而可能产生各种血流动力学改变，如同在酒精中毒者中所发现的那样。所述机制在多大程度上导致或可能加剧在酒精性疾病中观察到的众多其他紊乱，应进一步分析。
