Autor: |
Lee M; Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas., Aldred K, Lee E, Prince MD, Feldman M |
Jazyk: |
angličtina |
Zdroj: |
Gastroenterology [Gastroenterology] 1992 Nov; Vol. 103 (5), pp. 1467-74. |
DOI: |
10.1016/0016-5085(92)91166-2 |
Abstrakt: |
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. |
Databáze: |
MEDLINE |
Externí odkaz: |
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