Aim: The study of alkaline gastric secretion in health and disease and its changes in response to blockers of H2-histamine receptors.
Materials and methods: The trial enrolled 74 patients with duodenal ulcer (DU), 28 patients with chronic gastric (CG) and 16 healthy controls. The secretion was studied initially, in administration of ranitidine, in stimulation with hydrochloric acid.
Results: DU patients demonstrated a significant reduction of gastric secretion of bicarbonates in the basal and stimulated phases and a 3-fold decrease in the proportion alkaline/acid secretion. There was also a trend to acidosis. Administration of H2-histamine receptors provided recovery of acid-alkaline balance.
Conclusion: Bicarbonate deficiency is an important element of duodenal ulcer pathogenesis.