EFFECTS OF AMMONIA ON HELICOBACTER-PYLORI-ASSOCIATED GASTRIC DISEASE

Objectives: To clarify the effects of ammonia in Helicobacter pylori-a ssociated gastric mucosal injury. Design: We studied the effects of am monia on acute gastric mucosal injury, gastric mucosal energy metaboli sm and healing of ulcers in rats. Methods: Various concentrations of a mmonia were administered orally to the rats and 30 min later gastric m ucosal injuries were investigated. The changes in gastric mucosal ener gy metabolism were investigated serially to determine the cause-effect relationship. The effect of ammonia on gastric mucosal mitochondrial oxygen consumption was investigated using a Clark-type oxygen electrod e. The effect of ammonia on the healing of acetic acid-induced gastric ulcers was investigated histologically. Results: An oral administrati on of ammonia at doses at or above 120 mmol/l caused acute gastric muc osal injury in a dose-dependent manner. This injury was preceded by de creases in energy charges and in ATP levels in the gastric mucosa. The ammonia directly inhibited oxygen consumption in gastric mucosal cell s, and may therefore cause acute gastric mucosal injury by impairing e nergy metabolism. When ammonia was administered in drinking water at 1 2 mmol/l there was a significant delay in the healing of gastric ulcer s, especially those located in the antrum. Conclusion: The ammonia pro duced by H. pylori may contribute to the development of gastric mucosa l injury, and may also affect the healing process of acetic acid-induc ed gastric ulcers by impairing mucosal energy metabolism.