We studied the chronic effect of ammonia, which is one of the pathogenic factors of Helicobacter pylori in gastroduodenal diseases, on the healing of acetic acid-induced gastric ulcers in rats with special reference to the collagen metabolism. Rats were given either tap water or 0.1 or 0.02% ammonia solution before and after ulcer induction. We measured the ulcer index, hydroxy-proline concentrations and type III collagen/total hydroxyproline ratios in the ulcer base. Epithelialization was achieved 4 weeks later under the influence of ammonia. Nevertheless, ammonia treatment significantly increased the collagen deposition in the ulcer base compared with the nonammonia treatment group, 4 weeks after ulcer induction. In the nonammonia treatment group, the type III collagen/total hydroxyproline ratio decreased 3 weeks after ulcer induction. On the contrary, in the groups treated with ammonia throughout the experiment, type III collagen/total hydroxyproline ratio remained high until 4 weeks after ulcer induction. In conclusion, intragastric ammonia delayed the ulcer healing process in its early phase, but did not affect the achievement of re-epithelialization. However, it disturbed the collagen metabolism in the ulcer base. Excessive deposition of collagen and an abnormally high proportion of its immature type may be unfavorable for ulcer healing. These findings may explain in part why H. pylori-màuccå ulcer is so difficult to trea