1985
DOI: 10.1111/j.1476-5381.1985.tb12919.x
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Comparison of the action of cholinomimetics and pentagastrin on gastric secretion in dogs

Abstract: Stimulation of acid secretion by muscarinic cholinomimetic agents depended on the periodic interdigestive activity of the stomach. This explains the peak and following fade. Pentagastrin stimulated gastric secretion after a fixed interval and did not depend on the interdigestive activity. Neither gastrin nor methacholine directly contracted the gallbladder in the doses used. A sustained secretion of gastric acid and pepsin, such as follows a meal, required both hormonal stimulation and gastric distension. The … Show more

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Cited by 10 publications
(6 citation statements)
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“…The suppression of prostaglandins synthesis by nonsteroidal anti-inflammatory drugs (NSAIDS), such as indomethacin, results in increased susceptibility to mucosal injury and gastroduodenal ulceration (Atay et al, 2000). Cholinomimetic agents (bethanechol) administered in association with NSAIDS have a synergistic effect on the gastric injury induced by increased secretion of acid and pepsin in the stomach (Rainsford, 1978;Magee et al, 1985). Significant and dosedependent inhibition of the gastric ulcer was observed from the pre-treatment with HE from Qualea grandiflora.…”
Section: Resultsmentioning
confidence: 95%
“…The suppression of prostaglandins synthesis by nonsteroidal anti-inflammatory drugs (NSAIDS), such as indomethacin, results in increased susceptibility to mucosal injury and gastroduodenal ulceration (Atay et al, 2000). Cholinomimetic agents (bethanechol) administered in association with NSAIDS have a synergistic effect on the gastric injury induced by increased secretion of acid and pepsin in the stomach (Rainsford, 1978;Magee et al, 1985). Significant and dosedependent inhibition of the gastric ulcer was observed from the pre-treatment with HE from Qualea grandiflora.…”
Section: Resultsmentioning
confidence: 95%
“…The model of NSAID-induced gastric lesions employed in this study has been developed in mice [6,17] in whom the gastric mucosa is sensitized towards the ulcerogenic effects of the NSAIDs by co-treatment with the cholinomimetic, bethanechol chloride (acetyl-fl-methyl choline chloride), so as to stimulate acid and pepsin production in the stomach [7]. A marked enhancement of NSAID-induced lesions is produced with bethanechol when given at an optimal dose of 5 mg/kg i.p.…”
Section: Methodsmentioning
confidence: 99%
“…40) Cholinomimetic agent (bethanechol) administered in association with NSAIDS have a synergistic effect on the gastric injury induced by increased secretion of acid and pepsin in the stomach. 19,41) In the indomethacin/bethanechol-induced ulcer model, cimetidine (100 mg/kg), EEOH (50, 100, 250 mg/kg), FRF and FDF (100 mg/kg) significantly protected the gastric mucous against ulcer formation (Table 4), probably by a mechanism involving increased mucous production.…”
Section: Resultsmentioning
confidence: 99%