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Metabolic base production and mucosal vulnerability during acid inhibition in a mammalian stomach in vitro

Digestive Diseases and Sciences, ISSN: 0163-2116, Vol: 41, Issue: 5, Page: 964-971
1996
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Article Description

Acid inhibition increases gastric mucosal susceptibility to damage by luminal acid. This might be due to reduced metabolic CO and bicarbonate whereas, during normal acid, secretion cytoprotective CO/HCO 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 CO supply. Without acid inhibition there was no mucosal damage at any level of serosal CO/HCO supply. Acid inhibition reduced metabolic CO 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% CO supply completely replaced the reduction in metabolic CO, it did not protect against mucosal damage. Overreplacement by 5% serosal CO/HCO was required to prevent damage. There was no correlation between luminal CO/HCO output and mucosal damage. The protection by endogenous or exogenous CO/HCO appears to act intracellularly rather than by intragastric or intercellular neutralization.

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