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Abstract
The pathogenesis of acidic reflux esophagitis was investigated in an experimental
model with special emphasis on the role of lumen-to-mucosa diffusion of H+ in the pathogenetic mechanism. Esophageal damage was produced by perfusing an isolated
segment of rabbit esophagus in situ with three injurious endogenous secretions of
the upper gastrointestinal tract (taurocholate, 10 mM; pepsin, 2500 U/ml; lysolecithin,
2 mg/ml) with and without acid (HCl, 10 to 150 mM). The seventy of mucosal damage
was assessed using as indicators of mucosal integrity transmucosal potential difference,
net flux of Na+, and mucosal permeability to two neutral molecules of different sizes—3H-H2O and 14C-erythritol. The data indicate that although the presence of luminal acid is needed
for mucosal damage to develop, there is no relationship between the severity of the
damage and the magnitude of the lumen-to-mucosa diffusion of H+. Even markedly increased diffusion of H+ alone, induced by an unphysiologically high concentration of luminal acid (300 mM
HCl), had only a minor influence on mucosal integrity, whereas all three test agents
were able to cause severe mucosal damage in association with much lower rates of H+ diffusion. Furthermore, the seventy of the mucosal damage caused by an individual
test agent was not dependent on the HCl concentration used (and hence on the magnitude
of lumen-to-mucosa diffusion of H+). The data suggest that esophageal mucosal damage caused by taurocholate, pepsin,
or lysolecithin in the presence of luminal acid is due to the direct action of the
agent itself rather than to excessive accumulation of luminal H+ into the mucosal tissue.
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Article info
Publication history
Accepted:
February 10,
1982
Footnotes
☆Supported by a grant from the Sigrid Jusélius Foundation, Helsinki, Finland.
Identification
Copyright
© 1982 Published by Elsevier Inc.
