Article: article from journal or magazin.
Case report (case report): feedback on an observation with a short commentary.
Metabolic base production and mucosal vulnerability during acid inhibition in a mammalian stomach in vitro.
Digestive Diseases and Sciences
Publication types: Comparative Study ; In Vitro ; Journal Article ; Research Support, Non-U.S. Gov't
Acid inhibition increases gastric mucosal susceptibility to damage by luminal acid. This might be due to reduced metabolic CO2 and bicarbonate whereas, during normal acid, secretion cytoprotective CO2/HCO3- production parallels acid production. Metabolic activity and mucosal damage caused by luminal acid perfusion was determined in an in vitro mouse stomach, with and without acid inhibition, and at 0%, 1%, or 5% serosal CO2 supply. Without acid inhibition there was no mucosal damage at any level of serosal CO2/HCO3- supply. Acid inhibition reduced metabolic CO2 production by 29% (P < 0.004) and resulted in microscopic damage 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. Overreplacement by 5% serosal CO2/HCO3- was required to prevent damage. There was no correlation between luminal CO2/HCO3- output and mucosal damage. The protection by endogenous or exogenous CO2/HCO3- appears to act intracellularly rather than by intragastric or intercellular neutralization.
Acid-Base Equilibrium/drug effects, Adenosine Triphosphatases/antagonists & inhibitors, Animals, Bicarbonates/metabolism, Carbon Dioxide/metabolism, Enzyme Inhibitors/pharmacology, Female, Gastric Acid/secretion, Gastric Mucosa/drug effects, Gastric Mucosa/metabolism, Hydrogen-Ion Concentration, Imidazoles/pharmacology, Mice, Serous Membrane/drug effects, Serous Membrane/metabolism
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