BACKGROUND AND AIMS: Administration of omeprazole to healthy volunteers was recently reported to increase proximal duodenal mucosalbicarbonate secretion. As human oesophagus also secretes bicarbonate, the hypothesis was tested that omeprazole may stimulate oesophagealbicarbonate secretion and thus contribute to the therapeutic efficacy of the drug in gastro-oesophageal reflux disease. SUBJECTS ANDMETHODS: In nine healthy volunteers, oesophageal "steady state" perfusion of a 10 cm open segment of distal oesophagus was performed twice inrandom order. The volunteers were pretreated with either 60 mg/day omeprazole for three days and 80 mg intravenous omeprazole before perfusionor 600 mg/day ranitidine for three days and 50 mg/h intravenously during the perfusion. Saliva and samples of aspirate from the perfusedoesophagus and stomach were collected and bicarbonate concentrations were measured. RESULTS: The median rates (95% confidence intervals)of intrinsic oesophageal bicarbonate secretion, corrected for contaminating salivary and gastric bicarbonate, were 89 (33-150) and 121 (63-203)mumol/h/10 cm (p > 0.5) in omeprazole and ranitidine treated subjects respectively. Salivary and gastric bicarbonate contaminating the oesophagusaccounted for 14% and 3%, respectively, of total oesophageal bicarbonate output. CONCLUSIONS: Bicarbonate secretory capacity of the humanoesophagus is less than previously assumed, and the clinical relevance of intrinsic oesophageal bicarbonate for mucosal defence may be overestimated. As omeprazole and ranitidine did not affect bicarbonate secretion differently there was no evidence that omeprazole acts on icarbonate secretory cells in the oesophageal mucosa.
|Publication status||Published - 1997|