Abstract
Pentagastrin infused intravenously in a dose of 16 μg per kg body weight per hour, caused submaximal gastric acid response from gastric fistulas, and produced, after a period of 24 to 36 hours, acute duodenal ulcers in cats.
Increasing the dose of the stimulant in the same limits of infusion time did not augment the ulcerogenic action of pentagastrin, whereas the rate of appearance and the magnitude of the ulcer area rose along with the duration of the stimulant infusion.
Diversion of bile and pancreatic juice to jejunum did not change basal acid output or the dose response curve to pentagastrin, but facilitated the ulcer formation.