The aetiology of gastric ulceration induced by electrical vagal stimulation in rats

Abstract

Histamine and serotonin levels in gastric secretion and the effects of pharmacological antagonists were studied in rats in which stomach ulceration was induced by electrical vagal stimulation. Electrical vagal stimulation (2 and 5 V) produced a graded increase in haemorrhagic glandular mucosal ulcers. NaHCO3 perfusion completely neutralised the increased acid output but failed to prevent ulceration. Atropine inhibited gastric mast cell degranulation as well as histamine and serotonin release. Diphenhydramine, atropine and sub-diaphragmatic vagotomy antagonised the increase in intragastric pressure. Diphenhydramine, cimetidine, atropine or vagotomy but not methysergide reduced ulcer severity. It is concluded that gastric acid and serotonin do not play an important role in glandular ulceration induced by electrical vagal stimulation. The lesions probably result from increased intragastric pressure and release of gastric histamine which stimulates H1 and H2 receptors in the stomach. The similarities between the aetiologies of glandular ulcers due to electrical vagal stimulation and to stress are also discussed.