Mucus and bicarbonate secretion in the stomach and their possible role in mucosal protection How the gastric mucosa is able to withstand intraluminal acid, which can attain concentrations approaching 155 mM H+ under conditions of maximal stimulation, remains an unanswered question. The concept of the gastric mucosa as a limiting barrier to ion diffusion developed from an appreciation that the concentration of electrolytes in the stomach varies with the rate of secretion. Thus gastric juice has a high Na+ and a low H+ concentration at low secretory rates, while at high secretory rates the reverse is found.1 In addition it is well known that a reduction in H+ and gain in Na+ occurs after instillation of exogenous acid into the ligated stomach or gastric pouch.23 Teorell4 considered the gastric mucosa as a diffusion barrier and described events at the mucosal surface in terms of an exchange diffusion between H+ in the lumen and Na+ in the mucosa. In contrast, Hollander5 proposed a two component barrier consisting of the mucus layer lining the gastric mucosa together with the subjacent layer of epithelial cells and suggested that the reduction in H+ concentration resulted from dilution and neutralisation by a Na+ containing non-acid secretion or leakage of interstitial fluid.
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Allen et al. (1980) studied this question.
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