Aggravation by the Capsaicin-Treatment of Gastric Antral Ulcer Induced by the Combination of 2-Deoxy-D-Glucose, Aspirin and Ammonia in Rats

Abstract

The effect of capsaicin-sensitive nerve degeneration (capsaicin-treatment) was investigated on the antral ulcer induction by the combined administration of 2-deoxy-D-glucose (2-DG; 200 mg/kg, i.v.), aspirin (200 mg/kg, p.o.) and 1% ammonia solution (10 ml/kg, p.o.) in male Sprague-Dawley rats. On the 2nd day after ulcer induction, erosive lesions were seen in the corpus, and ulcers penetrating into the muscularis mucosae were also seen in the antrum. In the capsaicin-treated rats, the antral ulcer was significantly aggravated as compared with that in capsaicin non-treated rats, although no difference was noted in the formation of corpus lesions between capsaicin-treated rats and non-treated rats. Acid output was investigated in pylorus ligated rats. 2-DG significantly increased the acid output. A significant increase in acid output was also observed in capsaicin-treated rats, and this increase tended to be augmented by the additional treatment with 2-DG. Atropine sulfate inhibited the significant increase in acid output of the capsaicin-treated rats. In all rats, both capsaicin-treated and pylorus-ligated, 2-DG induced antral ulcers that penetrated into the muscularis mucosae. From the above results, it was suggested that capsaicin-sensitive nerve degeneration modifies the gastroprotective ability in the antral mucosa to a greater extent than in the fundic mucosa, and this aggravation may be caused by activation of the vagus nerve, although the role of acid is not completely excluded.