Objectives: The aim of the present study was to assess the relative contribution of duodenal and biliopancreatic bicarbonate secretion to acid neutralization in the duodenum, in basal conditions, during stimulation by PGE2 and during acid infusion in the duodenum.
Methods: Forty rats were anaesthetized and the duodenum was infused with 0.9% saline. Bicarbonate originating from duodenal mucosa and from biliopancreatic secretion was independently collected and measured. In neutralization studies, HCl was infused in the duodenum, and the amount of residual acid escaping from the duodenum was determined with and without bile and/or pancreatic juice diversion.
Results: Basal duodenal and biliopancreatic bicarbonate outputs were respectively 10.0 +/- 0.66 and 2.4 +/- 0.31 mumol/10 min. PGE2 increased duodenal mucosal bicarbonate by about 100%. Eighty-five percent of infused HCl was neutralized by duodenal mucosal bicarbonate. In neutralizing the remaining 15%, pancreatic secretion was slightly predominant, 46% for a HCl concentration of 5 mM and 71% for a HCl concentration of 40 mM.
Conclusions: These results shows that in the anaesthetized rat, available bicarbonate in the duodenal lumen and HCl neutralization ability are mainly dependent upon bicarbonate secreted by the duodenal mucosa.
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