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摘要
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.
