Premium
Omeprazole prevents indomethacin‐induced gastric ulcers in rabbits
Author(s) -
LEE M.,
KALLAL S. M.,
FELDMAN M.
Publication year - 1996
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1046/j.1365-2036.1996.34176000.x
Subject(s) - omeprazole , medicine , proton pump inhibitor , prostaglandin e2 , prostaglandin , gastric acid , pharmacology , gastroenterology , stomach , subcutaneous injection , indometacin , gastric mucosa , prostaglandin e , enzyme inhibitor , chemistry , prostaglandin endoperoxide synthase , enzyme , biochemistry
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 E 2 (PGE 2 ) formation. Conclusion : We conclude from these observations that gastric acid plays a critical role in the formation of indomethacin‐induced gastric ulcers in rabbits.