Pathogenesis of duodenal ulcer. Gastric hyperacidity caused by propionitrile and cysteamine in rats.
Cysteamine and propionitrile, experimental duodenal ulcerogens, stimulated gastric acid secretion in the rat. Gastric acid secretion was measured by two separate methods, the conventional pylorus ligation technique and a non-invasive technique based on the pH dependent liberation of azure A from azuresin in the stomach with subsequent excretion of the liberated dye in the urine. Volume, acid concentration and acid content of gastric fluids aspirated immediately before the pylrous ligation were markedly increased 1,4 and 7 hours after a single dose of either cysteamine or propionitrile. Both acid concentration and acid output of gastric contents collected 30 minutes after pylorus ligation were also significantly elevated 1.5 hours after propionitrile and 4.5 hours after cysteamine. Significant increases in gastric acid secretion after these chemicals were also measured by the non-invasive technique which demonstrated a 4 to 6 fold increase in 24 hour urinary azure A output in rats injected with either propionitrile or cysteamine. Enhanced gastric acid output may play an important role in the pathogenesis of duodenal ulcer produced by propionitrile and cysteamine.
D000818:Animals; D001399:Azure Stains / Q000652:urine; D003543:Cysteamine / Q000494:pharmacology*; D004381:Duodenal Ulcer / Q000139:chemically induced* / Q000473:pathology; D005260:Female; D005745:Gastric Acidity Determination; D005750:Gastric Juice / Q000187:drug effects / Q000378:metabolism*; D008026:Ligation; D009570:Nitriles / Q000494:pharmacology*; D011708:Pylorus / Q000502:physiology; D051381:Rats; D013268:Stimulation, Chemical; D013997:Time Factors
D001399:Azure Stains; D009570:Nitriles; D003543:Cysteamine