Effects of protective drugs on gastric alkaline secretion in man

This study was designed to determine the effects of sucralfate, De-Nol, and Maalox 70 on gastric HCO3 secretion in 34 healthy humans. Alkaline secretion was measured after pretreatment with ranitidine to abolish 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 perfusates. Addition of sucralfate or De-Nol resulted in increments of gastric HCO3 secretion, reaching about 45% and 59%, respectively, of the maximal HCO3 response to 16,16-dimethyl PGE2 (dmPGE2). The highest response to Maalox 70 reached about 21% of dmPGE2 maximum. These effects of sucralfate, De-Nol, and Maalox 70 were accompanied by a significant increase in luminal release of PGE2. Pretreatment with atropine reduced basal and, in part, sucralfate-, De-Nol-, and Maalox 70-induced alkaline secretion, whereas pirenzepine did not affect this secretion. Aspirin reduced the release of PGE2 by about 80% and suppressed almost completely the gastric HCO3 response to sucralfate, De-Nol, and Maalox 70. This study provides evidence that sucralfate, De-Nol, and Maalox 70 stimulate gastric alkaline secretion via a prostaglandin-dependent mechanism.