Effects of Protective Drugs on Gastric Alkaline Secretion in Man

Abstract

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 PGE_z 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.

Key Words:

• Alkaline secretion
• De-Nol®
• gastric secretion
• Maalox 70®
• prostaglandin E₂
• sucralfate