Cysteamine induced duodenal ulcer

The duodenal ulcerogenic action of propionitrile and cysteamine was confirmed and extended by several authors (J, 8, 25-32). The model, especially the rapidly developing cysteamine-induced duodenal ulcer, was actually introduced in several laboratories to routinely test drugs for anti-ulcer activity (7.8,27.33). The cysteamine model, a simple, fast, and inexpensive procedure, became especially useful after a chronic form of duodenal ulcer was developed ( ) and similarities between the model and human duodenal ulceration were noted (7-10). 

Recent data in our laboratories indicated the possible involvement of central and peripheral dopamine binding sites in the pathogenesis of duodenal ulceration. Structure activity studies with duodenal ulcerogens implicated dopamine as a putative mediator and/or modulator in duodenal ulceration. Using the cysteamine- or propionitrile-induced duodenal ulcer model in rats, we found that dopamine agonists (e.g., bromocriptine, lergotrile,... 

On the other hand, dopamine antagonists (e.g. haloperidol or pimozide) aggravated the duodenal ulcers and mortality after cysteamine administration. The chemically induced duodenal ulceration was associated with changes in the sensitivity and number of dopamine receptors in the gastric and duodenal mucosa and mus-cularis propria (Szabo and Neumeyer 1983). 

The actions of these drugs are not specific to cysteamine since the intensity of propionitrile-induced acute duodenal ulcers was also significantly diminished after pretreatment with bromocriptine or lergotrile (Table I). 

Administration of cysteamine enhances inflammatory reaetions. Cysteamine is used to induce experimental duodenal ulcer model using animals. 

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