RESUMO
Objective To study the role of vascular mediators in the pathogenesis of hepatopulmonary syndrome in rats. Methods Male Sprague-Dawley (SD) rats were divided into four groups: SO (surgical control), IHPH (intrahepatic portal hypertension), PHPH (prehepatic) and PCS (portocaval shunt). Two weeks after pathological study, arterial blood gas and the concentrations of NO, glucagon, VIP and ET-1 in plasma and lung were determined. Results Lung structural alteration of rats induced by CCl 4 was of alveolar capillary dilation and angiogenesis, thickened alveolar septa and decreased alveolar capacity. There was no inflammation, edema, fibrosis, alveolar collapse and hyaline membrane formation in lung of all rats. PaO 2 ( mm?Hg)decreased more significantly in IHPH (73.85?6.51) rats than in PHPH (972?9?1.33), PCS (95.23?2.22) and SO rats (99.05?0.75). The level of lung NO of IHPH (19.78?5.33) was significantly increased than those of PHPH (13.21?3.99) and PCS (13.89?3.16) whose level in lung homogenate increased than those of SO (8.71?1.68). There was no difference of Glu and VIP levels in lung among all rats. The level of lung ET-1 in IHPH was significantly decreased than other rats. Conclusion Increased NO levels and decreased ET-1 levels in lung of HPS rats cause alveolar dilation and angiogenesis leading to mismatched ventilation-perfusion, and decrease of PaO 2.