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It is postulated the pulmonary injury in acute necrotizing pancreatitis could be due to oxygen-derived free radicals released during the attack of acute pancreatitis. To elucidate the relationship between oxygen-derived free-radicals and the degree of pulmonary injury in acute necrotizing pancreatitis, lipid peroxide (LPO) in lung tissuses, bronchoalveolar lavage fluid and serum were measured in 10 adult Mongrel dogs with acute necrotizing pancreatitis induced by injection of 5% sodium taurocholate into the pancreatic duct. Compared with the controis (n=10), the weight of lung was increased (241.2±33.7 g vs 121.2±51.4 g, P<0.05). LPO of bronchoalveolar lavage fluid (BALF) was higher (3.56±1.64μmol/L vs 0.75± 0.31μmol / L, P<0.05), LPO in peripheral and portal vein 10 hours after induction of acute pancreatitis was also significantly increased. The LPO content of lung tissue was not higher than that of the control group, but hemorrhage within alveolar space and infiltration by polymorphonuelcar and
It is postulated the pulmonary injury in acute necrotizing pancreatitis could be due to oxygen-derived free radicals released during the attack of acute pancreatitis. Lipid peroxide (LPO) in lung tissuses, bronchoalveolar lavage fluid and serum were measured in 10 adult Mongrel dogs with acute necrotizing pancreatitis induced by injection of 5% sodium taurocholate into the pancreatic duct. Compared with the controis (n = 10), the weight of The lung was increased (241.2 ± 33.7 g vs 121.2 ± 51.4 g, P <0.05). LPO of bronchoalveolar lavage fluid (BALF) was higher (3.56 ± 1.64 μmol / L vs 0.75 ± 0.31 μmol / in peripheral and portal vein 10 hours after induction of acute pancreatitis was also significantly increased. The LPO content of lung tissue was not higher than that of the control group, but hemorrhage within alveolar space and infiltration by pol ymorphonuelcar and