PURPOSE: We investigated the effects of the gastric mucosal blood flow on the pathophysiology of ammonia-induced gastric mucosal damage. DESIGN: The study was designed to show whether the damaging effect of ammonia, a product of Helicobacter pylori urease, on the gastric mucosa is increased by the decrease in gastric mucosal blood flow in rats subjected to ischemia. RESULTS: Although ammonium chloride at concentrations of 15-60 mmol/l produced no significant macroscopical lesion in normotensive rats, it caused severe macroscopic hemorrhagic gastric lesions in the stomachs of rats subjected to ischemia. Exposure of the stomach to the combination of ischemia and ammonium chloride (60-600 mmol/l, pH adjusted to 7-9 with sodium hydroxide) produced macroscopic hemorrhagic lesions. However, exposure of the mucosa to the combination of ischemia and sodium hydroxide (60-600 mmol/l, pH was reduced to 7-9 with hydrochloric acid) produced no significant lesions. CONCLUSIONS: These results indicate that the mucosal lesions observed in patients infected with H. pylori are not caused by the alkalinity of H. pylori-produced ammonia and suggest that concomitant infection with H. pylori in the ischemic stomach may lead to the development of ulceration in these patients.
PURPOSE: We investigated the effects of the gastric mucosal blood flow on the pathophysiology of ammonia-induced gastric mucosal damage. DESIGN: The study was designed to show whether the damaging effect of ammonia, a product of Helicobacter pylori urease, on the gastric mucosa is increased by the decrease in gastric mucosal blood flow in rats subjected to ischemia. RESULTS: Although ammonium chloride at concentrations of 15-60 mmol/l produced no significant macroscopical lesion in normotensive rats, it caused severe macroscopic hemorrhagic gastric lesions in the stomachs of rats subjected to ischemia. Exposure of the stomach to the combination of ischemia and ammonium chloride (60-600 mmol/l, pH adjusted to 7-9 with sodium hydroxide) produced macroscopic hemorrhagic lesions. However, exposure of the mucosa to the combination of ischemia and sodium hydroxide (60-600 mmol/l, pH was reduced to 7-9 with hydrochloric acid) produced no significant lesions. CONCLUSIONS: These results indicate that the mucosal lesions observed in patients infected with H. pylori are not caused by the alkalinity of H. pylori-produced ammonia and suggest that concomitant infection with H. pylori in the ischemic stomach may lead to the development of ulceration in these patients.