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. 1987 Dec;28(12):1557–1563. doi: 10.1136/gut.28.12.1557

De-Nol stimulates gastric and duodenal alkaline secretion through prostaglandin dependent mechanism.

S J Konturek 1, J Bilski 1, N Kwiecien 1, W Obtuløwicz 1, B Kopp 1, J Oleksy 1
PMCID: PMC1433922  PMID: 3480844

Abstract

This study was designed to determine the effects of colloidal bismuth subcitrate De-Nol on gastric HCO3- secretion in 24 healthy subjects and on gastric and duodenal HCO3- secretion in dogs with gastric and duodenal fistulae. Alkaline secretion was measured after pretreatment with ranitidine to abolish the H+ secretion using a constant perfusion aspiration system and back titration of the perfusates to the original pH 6.0. Luminal release of PGE2 was also measured in the gastric and duodenal perfusates. Addition of De-Nol in gradually increasing concentrations resulted in step wise increments in gastric HCO3- secretion in man and in dogs reaching, respectively, about 80% and 55% of the maximal HCO3- response to 16, 16dimethyl-PGE2 (dmPGE2). The duodenal HCO3- response to De-Nol in dogs reached 72% of the dmPGE2 maximum. These effects were accompanied by a significant increase in luminal release of PGE2. Pretreatment with atropine reduced basal and in part De-Nol induced alkaline secretion, whereas pirenzepine did not affect this secretion in man and dogs. Aspirin (in man) and indomethacin (in dogs) reduced the release of PGE2 by about 80% and suppressed almost completely the gastric and duodenal HCO3- response to De-Nol in these species. This study provides evidence that De-Nol stimulates gastroduodenal alkaline secretion through a prostaglandin dependent mechanism.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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