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The FASEB Journal, Vol 6, 825-831, Copyright © 1992 by The Federation of American Societies for Experimental Biology

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Experimental gastric mucosal injury: laboratory models reveal mechanisms of pathogenesis and new therapeutic strategies

GB Glavin and S Szabo
Department of Pharmacology and Therapeutics, University of Manitoba, Faculty of Medicine, Winnipeg, Canada.

Gastric ulcer is a multifaceted, pluricausal illness. Knowledge of the pathophysiology of gastric ulcer disease remains incomplete. Current pharmacological management of gastric ulceration is directed primarily at the reduction or neutralization of gastric acid secretion despite evidence that patients with this disease often exhibit normal gastric secretory activity. Attempts have been made to prevent or reduce gastric mucosal injury by cytoprotective agents without diminishing gastric acidity. We review several alternate explanations for the cause of gastric ulcers by examining various experimental models of gastric mucosal damage, including ethanol-, stress-, and nonsteroidal antiinflammatory drug-induced gastric lesions. We also discuss possible new strategies for the treatment of ulcer disease, particularly novel pharmacological targets arising from research conducted with these models. Growing realization that factors other than gastric secretion contribute significantly to the development of gastric ulcer disease prompts the conclusion that these same factors represent viable treatment alternatives.


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Copyright © 1992 by The Federation of American Societies for Experimental Biology.