Importance of gastric acid in gastric ulcer formation in rabbits with antibody-induced prostaglandin deficiency.
The role of gastric acid in the development of gastroduodenal ulcers in prostaglandin-deficient conditions is unclear. In the current study, the effect of the proton pump inhibitor omeprazole on the formation of gastric ulcers was examined in a previously validated rabbit model of antibody-induced prostaglandin deficiency. Intragastric administration of 20 mg/kg omeprazole every 12 hours caused a profound suppression of gastric acidity (i.e., pH above 5 continuously). This same dose of omeprazole significantly reduced gastric ulcer formation induced by passive immunization with 6-keto-prostaglandin F1 alpha antibodies. It is concluded from these observations that gastric acid plays a critical role in the formation of gastric ulcers in rabbits with antibody-induced prostaglandin deficiency.
Lee
M
M
Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas.
Aldred
K
K
Lee
E
E
Prince
M D
MD
Feldman
M
M
D015121:6-Ketoprostaglandin F1 alpha / Q000502:physiology; D000704:Analysis of Variance; D000818:Animals; D000906:Antibodies / Q000276:immunology; D003429:Cross Reactions; D005744:Gastric Acid / Q000502:physiology*; D005747:Gastric Fistula; D005753:Gastric Mucosa / Q000378:metabolism; D007116:Immunization, Passive; D009853:Omeprazole / Q000494:pharmacology; D010437:Peptic Ulcer / Q000188:drug therapy / Q000209:etiology*; D011453:Prostaglandins / Q000172:deficiency* / Q000502:physiology; D011817:Rabbits; D013270:Stomach / Q000473:pathology
D000906:Antibodies; D011453:Prostaglandins; D015121:6-Ketoprostaglandin F1 alpha; D009853:Omeprazole