Experimental esophagitis in a rabbit model: Clinical relevance

Lawrence F. Johnson, John W. Harmon

Research output: Contribution to journalArticle

Abstract

Esophagitis occurs in patients with excessive acid and/or alkaline gastroesophageal reflux. This observation prompted us to develop a continuously perfused in vivo rabbit esophageal model to examine the potential for different endogenous injurious agents to cause H+ back diffusion and morphologic eviderice of esophagitis. We found that Hel at physiologic pH values did not break the mucosal barrier to H+ back diffusion or cause esophagitis. Bile salts at physiologic concentrations in both an acid or alkaline perfusate broke the mucosal barrier and caused H+ back diffusion, but failed to cause a inorphologic injury consistent with clinical reflux esophagitis, Instead, proteolytic enzymes, such as pepsin in an acid environment and trypsin in an alkaline environment, caused a severe hemorrhagic erosive esophagitis consistent with that seen clinically. We feel new therapeutic strategies for the treatment of reflux esophagitis should be directed at proteolytic enzymes rather than only HCI or bile salts, Finally, we showed sucralfate to be a mucosal protectant against the acid-pepsin injury.

Original languageEnglish (US)
Pages (from-to)26-44
Number of pages19
JournalJournal of clinical gastroenterology
Volume8
DOIs
StatePublished - Jun 1986
Externally publishedYes

Keywords

  • Acid
  • Bile salts
  • Clinical relevance
  • Experimental esophagitis
  • Pepsin
  • Rabbit esophageal model
  • Trypsin injuries

ASJC Scopus subject areas

  • Gastroenterology

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