title: [Experimental cirrhosis induced by carbon tetrachloride inhalation: adaptation of the technique and evaluation of lipid peroxidation].
abstract: 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 oxygen species play an important role in the pathogenesis of liver fibrosis.
  
  
  OBJECTIVE
  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 hematoxilineosin technique in different moments of carbon tetrachloride inhalation (5th, 7th, 9th, 12th 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 histologic characteristics evaluation. For the lipid peroxidation analysis, thiobarbituric acid and QL techniques were used. Cytologic and bacteriologic parameters were analysed in the ascitic fluid.
  
  
  RESULTS
  Cirrhosis was established in 100% of carbon tetrachloride rats between the 12th 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 ascites.
  
  
  CONCLUSIONS
  The carbon tetrachloride inhalation method developed in this study is effective in cirrhosis induction and ascites formation, and the carbon tetrachloride cirrhosis physiopathogenesis is probably related to the oxidative stress installation.
authors.affiliation: Departamento de Fisiologia, Universidade Federal do Rio Grande do Sul-UFRGS, no Hospital Irmandade Santa Casa de Misericórdia de Porto Alegre (ISCMPA), Porto Alegre, RS.
authors.forename: R V
authors.initials: RV
authors.lastname: Cremonese
authors.forename: A A
authors.initials: AA
authors.lastname: Pereira-Filho
authors.forename: R
authors.initials: R
authors.lastname: Magalhães
authors.forename: A A
authors.initials: AA
authors.lastname: de Mattos
authors.forename: C A
authors.initials: CA
authors.lastname: Marroni
authors.forename: C G
authors.initials: CG
authors.lastname: Zettler
authors.forename: N P
authors.initials: NP
authors.lastname: Marroni
mesh_terms: D000280:Administration, Inhalation; D000818:Animals; D001202:Ascitic Fluid / Q000737:chemistry*; D002251:Carbon Tetrachloride; D004195:Disease Models, Animal; D015227:Lipid Peroxidation / Q000502:physiology*; D008054:Lipid Peroxides / Q000378:metabolism; D008106:Liver Cirrhosis, Experimental / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology; D008297:Male; D018384:Oxidative Stress / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar
chemical_list: D008054:Lipid Peroxides; D002251:Carbon Tetrachloride