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 HCO3actually enters cells in order to regulate int