Hyperosmolar glucose prevents stress ulceration in the rat restraint model despite inhibition of endogenous prostaglandins.

Stress ulceration continues to be a problem in critically ill surgical patients and occasionally occurs even when prophylaxis is attempted with standard agents. Tube feedings protect against ulceration in clinical settings. Many tube feeding formulas and intragastric 25 per cent glucose alone prevent gastric lesions in the rat restraint model. Endogenous cytoprotective prostaglandin release is stimulated by the application of hyperosmolar sugar solutions to the gastric mucosa. To determine whether all or part of the protection afforded by 25 per cent glucose is mediated through stimulation of endogenous prostaglandins, hyperosmolar glucose was tested in restrained rats with and without concurrent cyclo-oxygenase blockade. Intragastric hyperosmolar glucose protected against gross and microscopic gastric lesions, raised the blood glucose level and elevated the gastric mucosal pH. Although cyclo-oxygenase blockade alone worsened the lesions produced by restraint, blocking cyclo-oxygenase in the rats given 25 per cent glucose did not lessen the protective effect of hyperosmolar sugar. We conclude that endogenous prostaglandins are useful in gastric mucosal defense but are not necessary for the protection afforded by 25 per cent glucose. It is likely that providing glucose directly to the stressed gastric mucosa enhances several aspects of gastric mucosal defense.