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Dimaprit stimulation of gastric acid secretion in rhesus monkeys and dogs
Author(s) -
Russell James,
Becci Michels,
Mir G. Nabi
Publication year - 1987
Publication title -
drug development research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.582
H-Index - 60
eISSN - 1098-2299
pISSN - 0272-4391
DOI - 10.1002/ddr.430100205
Subject(s) - dimaprit , gastric acid , stimulation , medicine , ranitidine , stomach , fissipedia , agonist , endocrinology , secretion , antagonist , histamine h2 receptor , receptor
Tests were performed to characterize the gastric secretory effect of the H 2 agonist, dimaprit, in rhesus monkeys. Dose‐response studies were performed. The monkeys were chaired, and increasing doses of dimaprit (0.03 to 3.0 mg/kg hr) were infused intravenously. Gastric secretions were collected continuously through a nasogastric tube and were measured at 15‐min intervals. The completeness of collection was confirmed based on the recovery of an intragastric marker. Dimaprit dose dependently increased the total acid output (ED 50 = 0.198 mg/kg hr) and the volume of gastric secretion. Ranitidine (1 mg/kg hr, i.v.) shifted the dimaprit dose‐response curve to the right in a parallel fashion causing a 13‐fold increase in the ED 50 for acid output (2.54 mg/kg hr). Similarly, ranitidine competitively inhibited the secretory effect of dimaprit in the gastric fistula dog. In addition, when a single dose of dimaprit was infused over a 4‐hr period, both the monkey and dog exhibited a secretory plateau followed by a secretory “fade.” We conclude that the secretory effects of dimaprit are qualitatively similiar for rhesus monkeys and dogs.