title: [Experimental models for assessment of pulmonary alterations in hepatopulmonary syndrome].
abstract: OBJECTIVE
  The aim of this study was to identify the best experimental model in which to observe the pulmonary alterations characterizing hepatopulmonary syndrome (HPS).
  
  
  METHODS
  Male Wistar rats, with mean weight of 250 g, were used in four experimental models: inhaled carbon tetrachloride; intraperitoneal carbon tetrachloride; partial portal vein ligation; and bile duct ligation (BDL). The animals in all groups were divided into control and experimental subgroups. The following variables were measured: transaminase levels; blood gases; lipoperoxidation, using thiobarbituric acid reactive substances (TBARS) and chemiluminescence; and levels of superoxide dismutase (SOD) anti-oxidant activity. Anatomopathological examination of the lung was also performed.
  
  
  RESULTS
  There were statistically significant differences between the BDL control and BDL experimental groups: aspartate aminotransferase (105.3 +/- 43 vs. 500.5 +/- 90.3 IU/L); alanine aminotransferase (78.75 +/- 37.7 vs. 162.75 +/- 35.4 IU/L); alkaline phosphatase (160 +/- 20.45 vs. 373.25 +/- 45.44 IU/L); arterial oxygen tension (85.25 +/- 8.1 vs. 49.9 +/- 22.5 mmHg); and oxygen saturation (95 +/- 0.7 vs. 73.3 +/- 12.07%). Lipoperoxidation and antioxidant activity also differed significantly between the two BDL groups (control vs. experimental): TBARS (0.87 +/- 0.3 vs. 2.01 +/- 0.9 nmol/mg protein); chemiluminescence (16008.41 +/- 1171.45 vs. 20250.36 +/- 827.82 cps/mg protein); and SOD (6.66 +/- 1.34 vs. 16.06 +/- 2.67 IU/mg protein). The anatomopathological examination confirmed pulmonary vasodilatation in the BDL model. In the other models, there were no alterations that were characteristic of HPS.
  
  
  CONCLUSIONS
  The data obtained suggest that the BDL model can be used in future studies involving hepatic alterations related to oxidative stress and HPS.
authors.affiliation: Programa de Pós-graduação em Fisiologia, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brasil.
authors.forename: Rafael
authors.initials: R
authors.lastname: Vercelino
authors.forename: Juliana
authors.initials: J
authors.lastname: Tieppo
authors.forename: Luiz Albeto
authors.initials: LA
authors.lastname: Forgiarini Junior
authors.forename: Alexandre Simões
authors.initials: AS
authors.lastname: Dias
authors.forename: Claudio Augusto
authors.initials: CA
authors.lastname: Marroni
authors.forename: Norma Possa
authors.initials: NP
authors.lastname: Marroni
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001835:Body Weight; D003135:Common Bile Duct / Q000601:surgery; D020065:Hepatopulmonary Syndrome / Q000150:complications* / Q000503:physiopathology; D006976:Hypertension, Pulmonary / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D008099:Liver / Q000473:pathology / Q000503:physiopathology; D008106:Liver Cirrhosis, Experimental / Q000139:chemically induced / Q000473:pathology* / Q000503:physiopathology; D008111:Liver Function Tests; D008168:Lung / Q000473:pathology* / Q000503:physiopathology; D008297:Male; D009929:Organ Size; D018384:Oxidative Stress; D011169:Portal Vein / Q000503:physiopathology; D011659:Pulmonary Gas Exchange; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000975:Antioxidants; D013482:Superoxide Dismutase