Gastroduodenal Bicarbonate Secretion and its Response to Sucralfate

Abstract

Reduction of gastric acidity by ingestion of alkali has been used for decades to alleviate the symptoms and heal mucosal damage in peptic ulcer disease. The possibility that intrinsic secretion of alkali into surface mucus gel could protect gastric epithelium from acid attack was raised by Heatley some 40 years ago. However, because of limitations in experimental techniques, the existence of such alkali secretion was not proven until 25 years later. The advent of potent inhibitors of acid secretion coupled with the development of techniques for measuring small amounts of bicarbonate in vitro and in vivo has confirmed the existence of bicarbonate secretion by esophageal, gastric, and duodenal mucosa. This alkali secretion is capable of sustaining a significant pH gradient across gastric and duodenal surface mucus gel thereby reducing exposure of underlying cells to a damaging acid environment (Fig. 1). However, the importance of bicarbonate secretion to mucosal integrity within the proximal gut remains uncertain. It is conceivable that alkali secretion by the esophagus and duodenum plays a far greater role in protection against the smaller quantities of luminal acid found in these organs than in the stomach where luminal acidity is consistently higher and capable of overwhelming the mucus pH gradient. Stimulation of alkali secretion may have important implications for the management of peptic ulcer disease and may enhance ulcer healing or prevent ulcer recurrence without altering luminal acidity.