ENHANCED GASTRIC NITRIC-OXIDE SYNTHASE ACTIVITY IN DUODENAL-ULCER PATIENTS

Nitric oxide, the product of nitric oxide synthase in inflammatory cel ls, may have a role in tissue injury through its oxidative metabolism. Nitric oxide may have a role in the pathogenesis of duodenal ulcer an d may be one of the mechanisms responsible for the association between gastric infection with Helicobacter pylori and peptic disease. In thi s study, calcium independent nitric oxide synthase activity was detect ed in human gastric mucosa suggesting expression of the inducible isof orm. In 17 duodenal ulcer patients gastric antral and fundic nitric ox ide synthase activity was found to be two and 1.5-fold respectively hi gher than its activity in the antrum and fundus of 14 normal subjects (p < 0.05). H pylori was detected in the antrum of 15 of 17 duodenal u lcer patients and only in 7 of 14 of the control subjects. Antral nitr ic oxide synthase activity in H pylori positive duodenal ulcer patient s was twofold higher than in H pylori positive normal subjects (p < 0. 05). In duodenal ulcer patients antral and fundic nitric oxide synthas e activity resumed normal values after induction of ulcer healing with ranitidine. Eradication of H pylori did not further affect gastric ni tric oxide synthase activity. These findings suggest that in duodenal ulcer patients stimulated gastric mucosal nitric oxide synthase activi ty, though independent of the H pylori state, may contribute to the pa thogenesis of the disease.