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

Abstract:

: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.

journal_name

Dig Dis Sci

authors

Glauser M,Bauerfeind P,Feil W,Riegler M,Fraser R,Blum AL

doi

10.1007/BF02091538

subject

Has Abstract

pub_date

1996-05-01 00:00:00

pages

964-71

issue

5

eissn

0163-2116

issn

1573-2568

journal_volume

41

pub_type

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