objectives: in this study, we tested the hypothesis that hypertonic saline exerts anti-inflammatory effects by modulating hepatic oxidative stress in pancreatitis. introduction: the incidence of hepatic injury is related to severe pancreatitis, and hypertonic saline reduces pancreatic injury and mortality in pancreatitis. methods: wistar rats were divided into four groups: control (not subjected to treatment), untreated pancreatitis (nt, pancreatitis induced by a retrograde transduodenal infusion of 2.5% sodium taurocholate into the pancreatic duct with no further treatment administered), pancreatitis with normal saline (ns, pancreatitis induced as described above and followed by resuscitation with 0.9% nacl), and pancreatitis with hypertonic saline (hs, pancreatitis induced as described above and followed by resuscitation with 7.5% nacl). at 4, 12, and 24 h after pancreatitis induction, liver levels of inducible nitric oxide synthase (inos), heat-shock protein 70, nitrotyrosine (formation of peroxynitrite), nitrite/nitrate production, lipid peroxidation, and alanine aminotransferase (alt) release were determined. results: twelve hours after pancreatitis induction, animals in the hs group presented significantly lower inos expression (p<0.01 vs. ns), nitrite/nitrate levels (p<0.01 vs. ns), lipid peroxidation (p<0.05 vs. nt), and alt release (p<0.01 vs. ns). twenty-four hours after pancreatitis induction, nitrotyrosine expression was significantly lower in the hs group than in the ns group (p<0.05). discussion: the protective effect of hypertonic saline was related to the establishment of a superoxide-no balance that was unfavorable to nitrotyrosine formation. conclusions: hypertonic saline decreases hepatic oxidative stress and thereby minimizes liver damage in pancreatitis.