Abstract: To investigate the effect of endogenous nitric oxide (NO) on lung injury in acute pancreatitis in rats and its relationship to sulfhydryl compounds and lipid peroxidation. Methods: Acute pancreatitis lung injury model in rats was induced by retrograde sodium taurocholate (5%) infusion into the pancreatobiliary duct (1 mL/kg), and NGnitro Larginine (L-NNA) was used as the inhibitor of endogenous NO. The effect of endogenous NO on lung injury, lung tissue levels of sulfhydryl compounds and malonaldehyde (MDA, the end product of lipid peroxidation), were evaluated respectively. Results: Sodium taurocholate administration produced evident lung injury associated with acute necrosis pancreatitis in rats, a decrease of sulfhydryl compounds and a increase of MDA in lung tissue. Pretreatment with the NO inhibitor, L-NNA(12.5 mg/kg), significantly intensified lung injury, and resulted in a further increase of lung tissue MDA, but it had no effect on the lung tissue sulfhydryl compounds. Conclusion: Endogenous NO has the effect of lung protection, and its antioxidation may be responsible, at least in part, for the protective mechanisms. Sulfhydryl compound may not be involved in NO lung protection mechanisms.

Key words: nitric oxide, lung injury, acute pancreatitis, sulfhydrylcompound, oxygen free radicals