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Omeprazole prevents indomethacin-induced gastric ulcers in rabbits
1University of Texas Health Science Center at San Antonio, Southwestern Medical Center at Dallas, Dallas, Texas, USA.
Background:
The role of gastric acid in the development of non-steroidal anti-inflammatory drug (NSAID)-induced gastric ulcers is unclear. The aim of this study was to determine the effect of the proton pump inhibitor omeprazole on the formation of indomethacin-induced gastric ulcers in a rabbit model.
Methods:
Twenty-four rabbits were randomly divided into four groups and treated as follows: vehicle for indomethacin; vehicle for omeprazole; indomethacin (20 mg/kg b.d. subcutaneously for seven doses); and indomethacin plus omeprazole (both at 20 mg/kg b.d. subcutaneously for seven doses). On day 4 (after the seventh injection), rabbits were sacrificed, and gastric mucosal injury and prostaglandin formation were assessed.
Results:
Subcutaneous administration of 20 mg/kg omeprazole b.d. caused a profound suppression of gastric acidity (i.e. pH above 5.0 continuously). This same dose of omeprazole significantly reduced gastric ulcer formation induced by indomethacin despite significant (> 80%) inhibition of gastric mucosal prostaglandin E2 (PGE2) formation.
Conclusion:
We conclude from these observations that gastric acid plays a critical role in the formation of indomethacin-induced gastric ulcers in rabbits.