Leakage of HCO3- and mucosal restitution

Abstract

When the integrity of the gastric mucosa is destroyed, there is a large passive diffusion of interstitial HCO3- from the nutrient side to the luminal side of the tissue. In the absence of nutrient HCO3-, rapid repair of superficial mucosal injuries is slowed markedly down or does not take place at all. The effects of a high degree of luminal acidification, which prevents rapid repair, can be counteracted by high concentrations of nutrient HCO3-. The importance of nutrient HCO3- is emphasized by the finding that luminal acid may destroy both the fibrin network beneath which restitution occurs and the basal lamina along which viable cells must migrate to re-establish epithelial continuity. At the present time, it is not known whether the preventive effects of HCO3- against ulceration in a variety of systems are dependent upon leakage of HCO3- toward the surface, or whether nutrient HCO3- actually enters cells in order to regulate intracellular pH.