Cysteamine, administered as a single subcutaneous or oral dose, produced duodenal ulcers in rats within 24 h. At least 50 of the ulcers perforated at a dose of 425 mg/kg subcutaneously. Cysteamine-induced duodenal ulcers were prevented by an anti-cholinergic agent (methscopolamine bromide), by an antacid, by prostaglandins (PGE2 and 16,16-dimethyl PGE2), by prednisolone, and by interruption of the gastroduodenal transit (pylorus ligation). Fasting did not affect the incidence but reduced the severity (perforations) of the ulcers. The incidence and severity of ulcers was higher in female than in male rats. Desoxycorticosterone and ACTH did not influence the ulcers. Cysteamine inhibited gastric secretion (volume, acid and pepsin output, but not acid and pepsin concentration), in a dose-dependent manner. The pathogenesis of cysteamine-induced duodenal ulcers is unkown. Although cysteamine by itself is antisecretory, it requires some acid secretion and the passage of acid gastric contents over the duodenum to produce ulcers. Duodenal ulcers produced by cysteamine constitute the best model yet devised to test anti-ulcer agents. It is simple, rapid (24 h), and it responds to all antiulcer agents tested so far.
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