METABOLIC BASE PRODUCTION AND MUCOSAL VULNERABILITY DURING ACID INHIBITION IN A MAMMALIAN STOMACH IN-VITRO

Acid inhibition increases gastric mucosal susceptibility to damage by luminal acid, This might be due to reduced metabolic CO2 and bicarbona te whereas, during normal acid, secretion cytoprotective CO2/HCO3- pro duction parallels acid production, Metabolic activity and mucosal dama ge caused by luminal acid perfusion was determined in an in vitro mous e stomach, with and without acid inhibition, and at 0%, 1%, or 5% sero sal CO2 supply. Without acid inhibition there was no mucosal damage at any level of serosal CO2/HCO3- supply, Acid inhibition reduced metabo lic CO2 production by 29% (P < 0.004) and resulted in microscopic dama ge to 55% of the mucosal area and perforation in four of five stomachs (P < 0.05), Although, 1% CO2 supply completely replaced the reduction in metabolic CO2, it did not protect against mucosal damage. Overrepl acement by 5% serosal CO2/HCO3- was required mucosal damage. The prote ction by endogenous or exogenous CO2/HCO3- appears to act intracellula rly rather than by intragastric or intercellular neutralization.