Aspirin-induced gastric mucosal injury: lessons learned from animal models

Gastroenterology. 1989 Feb;96(2 Pt 2 Suppl):606-14. doi: 10.1016/s0016-5085(89)80056-3.


This review of the mechanisms by which aspirin causes gastric mucosal damage points to the involvement of two potential mechanisms. Aspirin, which inhibits cyclooxygenase, is rapidly deacetylated to salicylate. Salicylate is toxic to cells and affects mucosal barrier function, reduces cytosolic adenosine triphosphate, stimulates sodium transport, and increases proton dissipation from surface epithelial cells. Cyclooxygenase inhibition makes the gastric mucosa more susceptible to injury, inhibits mucus and bicarbonate secretion, alters the physicochemical nature of mucus, stimulates fundic but not antral [3H]thymidine incorporation, and reduces epithelial surface hydrophobicity. No single mechanism seems to be involved. It is likely, instead, that the toxic effects of salicylate and the effect of cyclooxygenase inhibition work in concert to render the mucosa more susceptible to injury, resulting in mucosal damage.

Publication types

  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Aspirin / pharmacokinetics
  • Aspirin / toxicity*
  • Cyclooxygenase Inhibitors
  • Disease Models, Animal
  • Gastric Mucosa / blood supply
  • Gastric Mucosa / drug effects*
  • Gastric Mucosa / enzymology
  • Prostaglandins / biosynthesis
  • Regional Blood Flow
  • Stomach Ulcer / chemically induced
  • Stomach Ulcer / metabolism
  • Stomach Ulcer / physiopathology*


  • Cyclooxygenase Inhibitors
  • Prostaglandins
  • Aspirin