BACKGROUND: Hepatopulmonary syndrome is formed by a triad of liver disease, intrapulmonary vascular dilatation and changes in blood gases. Its pathogenesis is not well defined, but it is speculated that a combination of factors, such as the imbalance of endothelin receptor responses, pulmonary microvascular remodeling, and genetic predisposition, leads to bacterial translocation and intrapulmonary vascular dilatation. AIM: To evaluate the myeloperoxidase activity in hepatopulmonary syndrome in rat model. METHOD: Twenty-nine rats were divided into control, sham and experimental hepatopulmonary syndrome groups. Was evaluated the myeloperoxidase activity and the experimental model used to induce hepatopulmonary syndrome was common bile duct ligation. RESULTS: The myeloperoxidase activity levels were significantly increased in the common bile duct ligation group as compared with the other groups. Myeloperoxidase activity was higher in the common bile duct ligation group than control group (p<0.05) and than sham group (p<0.05). CONCLUSION: The myeloperoxidase activity is increased in experimental hepatopulmonary syndrome in rats.
Hepatopulmonary syndrome; Animal model, experimental; Myeloperoxidase activity
