Secretory changes associated with chemically-induced duodenal ulceration: simultaneous measurements of acid, pepsin, base and pancreatic enzymes in rats with chronic gastric fistula.
Rats with chronic gastric fistula were used to study gastric and duodenal/pancreatic secretory changes evoked by chemical duodenal ulcerogens. Although the data demonstrate stimulation of gastric output of acid and pepsin by certain doses of cysteamine or propionitrile, cysteamine produced dose-response increases in acid secretion only during the 1st hour following administration. The base output was also elevated at most of the time intervals after cysteamine. Decreased alkaline secretion was only seen following propionitrile injection. Although hyperacidity at the ulcer site may occur during duodenal ulcerogenesis, these results suggest that direct stimulation of acid-pepsin secretion or depression of pancreatic alkaline output are not the primary mechanisms explaining the ulcerogenic action of cysteamine and propionitrile.
D000681:Amylases / Q000378:metabolism; D000818:Animals; D002908:Chronic Disease; D003543:Cysteamine; D004381:Duodenal Ulcer / Q000139:chemically induced / Q000201:enzymology / Q000378:metabolism*; D005260:Female; D005744:Gastric Acid / Q000378:metabolism*; D005747:Gastric Fistula / Q000201:enzymology / Q000378:metabolism*; D006863:Hydrogen-Ion Concentration; D009570:Nitriles; D010434:Pepsin A / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D014357:Trypsin / Q000378:metabolism
D009570:Nitriles; D003543:Cysteamine; C005557:propionitrile; D000681:Amylases; D014357:Trypsin; D010434:Pepsin A