[Gastric movements and reserpine-induced ulcer in rats]

Changes of gastric movements and ulcerogenic mechanisms in reserpine (6 mg/kg s.c.)-induced ulcer were studied in Wistar male rats weighing 180 to 220 g after fasting for about 20 hr. Under anesthesia with Nembutal (30 mg/kg i.p.), rats were fixed on their backs. The abdomen was incised and the stomach was exposed. Gastric movements of the fundic glandular area of greater curvature (A), the fundic-antral area of lesser curvature (B), and the neighboring area of pylorus (C) were recorded electromyographically after placing a small bipolar electrode of 1 mm distance on each area. Spontaneously, many higher amplitudes were found in area B and less found in area A. In area C, there were the least number of spikes and the lowest amplitudes. These gastric movements were inhibited until 1 hr after reserpine followed by a gradual increase in spikes and higher amplitudes. This increase was long-lasting and most marked in area B. Increased gastric movements due to reserpine were completely inhibited by atropine and vagotomy, moderately inhibited by hexamethonium and diphenhydramine, and only weakly inhibited by l-phenylephrine, l-isoproterenol, phentolamine, propranolol, metiamide, and methysergide. In reserpine-induced ulcer, ischemia occurred most markedly in area A, but erosions initiated from area B as reported previously. In area B, the gastric movements were most active, and the erosions were inhibited by the drugs which suppress gastric movements. These results suggest that reserpine-induced ulcer is due not only to the ischemia in the earlier stage, but also to the long-lasting hypermotility in the later stage.