Marshall W J, McLean A E
Br J Exp Pathol. 1969 Dec;50(6):578-83.
Cirrhosis has been produced in rats by a combination of carbon tetrachloride (CCl) and phenobarbitone administration. Hepatic microsomal cytochrome P-450 contents have been measured during the production of cirrhosis, and in established cirrhosis, after recovery from the acute effects of CCl has taken place. Cytochrome P-450 levels fall after CCl dosage but recover rapidly to near normal values in the early stages of the regime although later on they remain at a low level. In rats given 8 weeks to recover from the acute effects of the cirrhosis-producing regime, P-450 and pyramidon demethylation levels remained depressed in the more severely cirrhotic animals. The response to the inducing effect of phenobarbitone was diminished also. Liver water remained high in the more severely cirrhotic rats, but was near normal in those with less severe lesions. The basis of the changes observed is discussed and the features of experimental cirrhosis and clinical cirrhosis in man are compared.
通过给予四氯化碳（CCl）和苯巴比妥使大鼠产生肝硬化。在肝硬化形成过程中以及在已形成的肝硬化中，在四氯化碳的急性作用恢复后，对肝微粒体细胞色素P - 450含量进行了测定。给予四氯化碳后细胞色素P - 450水平下降，但在该方案的早期阶段迅速恢复到接近正常水平，尽管后期它们仍维持在低水平。在给予8周时间从致肝硬化方案的急性作用中恢复的大鼠中，在肝硬化更严重的动物中，P - 450和氨基比林去甲基化水平仍然降低。对苯巴比妥诱导作用的反应也减弱。在肝硬化更严重的大鼠中肝含水量仍然很高，但在病变较轻的大鼠中接近正常。讨论了观察到的变化的基础，并比较了实验性肝硬化和人类临床肝硬化的特征。
