Duodenal Mucosal Biocarbonate Secretion and its Importance to Mucosal Protection and Neutralization of Acid in the Duodenum

Duodenal ulcers develop as the result of an imbalance between aggressive and defensive factors in the duodenum. The reason for this imbalance is, however, unknown. Several defensive factors are believed to be active in the duodenum. Among these, mucosal bicarbonate secretion is considered to be of great importance. The evidence for this belief is, however, scarce.
The purpose of the present study was to determine if the human duodenum secretes bicarbonate and to examine the importance of the mucosal bicarbonate to the neutralization of acid in the lumen of the duodenum and in the immediate vicinity of the duodenal mucosa.
By using a multilumen tube it was confirmed that the human duodenal mucosa produces bicarbonate. The bicarbonate production of the human duodenal mucosa is of a magnitude sufficient, at least in theory, to account for the neutralization of a substantial part of the gastric acid secretion. Also by using a multilumen tube it was shown that inhibition of human duodenal mucosal bicarbonate secretion did not cause a reduction in the disappearance rate of acid in the intact human duodenum, suggesting that bicarbonate from the duodenal mucosa is not indispensable in the neutralization of acid in the intact human duodenum. However, measurements of plasma secretin concentrations suggested that the preserved neutralizing ability of the duodenum during inhibition of DMBS was the result of a compensatory increase in hepatic and pancreatic bicarbonate secretion. This indicates that DMBS normally plays a role in the in-lumen neutralization of acid in the duodenum but in the intact organism loss of DMBS can be compensated for by an increase in pancreatico-biliary bicarbonate secretion. This theory was tested by selectively measuring pancreatic, hepatic and duodenal mucosal bicarbonate secretion during inhibition/stimulation of DMBS in anaesthetized pigs. These studies demonstrated that compared to the other duodenal bicarbonate sources, i.e. the liver and the pancreas, the duodenum alone is capable of neutralizing a substantial part of an infused acid load. Furthermore the studies demonstrated that inhibition or stimulation of DMBS during duodenal acidification was accompanied by reverse compensatory changes in pancreatico-biliary bicarbonate secretion possibly due to a more/less effective stimulation of duodenal secretin cells. This finding suggests that DMBS does indeed participate in the regulation of intraduodenal pH. DMBS is, however, not likely to neutralize a major part of the in-lumen acid as inhibition/stimulation of DMBS did not have significant effects on the disappearance rate of large doses of acid. Finally, by using anaesthetized pigs it was demonstrated that stimulation of DMBS, without a concomitant increase in mucosa] blood flow, partially protects the duodenal mucosa against acid injury. It is concluded that the human duodenal mucosa secretes substantial amounts of bicarbonate. The bicarbonate secreted by the mucosa is of direct importance to the protection of the duodenal epithelium and of indirect importance to the neutralization of acid in the lumen of the duodenum.