Surfactant protein A is decreased in the lung of rats with hepatopulmonary syndrome

Abstract

PURPOSE:To evaluate surfactant protein A levels in an hepatopulmonary syndrome rat model. To date, there have been no studies aimed at evaluating surfactant levels in the setting of cirrhosis or hepatopulmonary syndrome. METHODS:A total of 35 rats were divided into control, sham, and experimental HPS groups. We evaluated surfactant protein A levels in rats and the experimental model designed to induce hepatopulmonary syndrome was common bile duct ligation. Statistical analysis was performed using GraphPad Prism Software ® . Differences were considered statistically significant when p<0.05. RESULTS:Lung homogenate of surfactant protein A levels were lower in the experimental hepatopulmonary syndrome and sham groups in comparison to the control group (p<0.05). Serum SP-A levels were the same in experimental hepatopulmonary syndrome and control groups but decreased in the sham group compared with the experimental groups (p<0.05). Myeloperoxidase activity was higher in the experimental hepatopulmonary syndrome group than the other two groups (p<0.05). CONCLUSION:Surfactant protein A is present in experimental hepatopulmonary syndrome and leads to an imbalance between serum and pulmonary levels due to systemic inflammatory response.

Impact of liver damage on blood-borne variables and pulmonary hemodynamic responses to hypoxia and hyperoxia in anesthetized rats

“…We previously indicated that ET-B receptors on the pulmonary smooth muscle cells play roles in the regulation of pulmonary vascular tone in animal model of liver cirrhosis [14]. Human studies have shown that reactive oxygen species (ROS) increase in POPH, but not in HPS [6,15], whereas, ROS are reportedly increased in animal models of HPS [7,[16][17][18]. Furthermore, high level of ROS may decrease the bioavailability of NO and lead to the constriction of pulmonary vessels [19].…”

“…However, due to the complexity in human studies, the classification of liver damage in patients may not be as accurate as the animal studies. HPS can be developed by a common bile duct ligation or drug administration in animals [7,18]. Nevertheless, a reliable method has not been introduced for the induction of POPH thus far.…”