Direct measurement of duodenal acid-pepsin exposure at site of ulceration in rats.
A new technique for the preparation of a chronic duodenal fistula in the rat is described. The effect of cysteamine and propionitrile on the acidity of duodenal contents was studied, and the degree of acidity correlated with the respective duodenal ulcerogenicity of these two compounds. After subcutaneous administration of cysteamine, reduced duodenal acid was seen for 2-4 h, followed by large increases continuing up to 12 h and declining thereafter. Oral cysteamine administration produced acid increases of rapid onset and shorter duration, accompanied by increased pepsin activity. The weak duodenal ulcerogen propionitrile did not affect duodenal acidity. Cimetidine markedly reduced the duodenal acidification induced by cysteamine, whereas the dopamine agonist bromocriptine did not affect acid delivery to the duodenum but reduced the pepsin activity in the duodenal contents by 50%. The duodenal fistula rat provides a new model system for studies on the pathogenesis of experimental duodenal ulcer.
D000818:Animals; D001971:Bromocriptine / Q000494:pharmacology; D002927:Cimetidine / Q000494:pharmacology; D003543:Cysteamine / Q000494:pharmacology; D004381:Duodenal Ulcer / Q000378:metabolism*; D004386:Duodenum / Q000502:physiology / Q000601:surgery; D005260:Female; D005402:Fistula; D005744:Gastric Acid / Q000378:metabolism*; D008722:Methods; D009570:Nitriles / Q000494:pharmacology; D010434:Pepsin A / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
D009570:Nitriles; D001971:Bromocriptine; D003543:Cysteamine; D002927:Cimetidine; C005557:propionitrile; D010434:Pepsin A