Background -- Long-term administration of carbon tetrachloride is an accepted experimental model to produce hepatic fibrosis. Oxidative stress has been postulated as a major molecular mechanism involved in carbon tetrachloride hepatotoxicity, where the reactive oxigen species play an important role in the pathogenesis of liver fibrosis. Aims - This study was conducted to evaluate the effectiveness of an experimental model of hepatic cirrhosis induced by carbon tetrachloride inhalation as well as the importance of lipid peroxidation and the characteristics of the ascitic fluid in this model. Methods - At first the hepatic histologic findings were assessed using the hematoxilin-eosin technique in different moments of carbon tetrachloride inhalation (5th, 7th, 9th, 12nd weeks). Later, at the end of 15 weeks of the study the rats were divided in three groups (control; control + phenobarbital; and carbon tetrachloride + phenobarbital) for lipid peroxidation, ascitic fluid and hystologic characteristics evaluation. For the lipid peroxidation analysis, thiobarbituric acid and QL techniques were used. Citologic and bacteriologic parameters were analysed in the ascitic fluid. Results - Cirrhosis was established in 100% of carbon tetrachloride rats between the 12nd and 15th weeks with an elevation in the lipid peroxidation carbon tetrachloride rats' livers. Ascitic fluid infection was observed in one of seven rats who has developed ascitis. Conclusions - The carbon tetrachloride inhalation method developed in this study is effective in cirrhosis induction and ascitis formation, and the carbon tetrachloride cirrhosis physiopathogenesis is probably related to the oxidative stress instalation.
Liver cirrhosis, experimental; Carbon tetrachloride; Oxidative stress; Ascites
