GASTRIC CYTOPROTECTION BY PROSTAGLANDINS, RANITIDINE, AND PROBANTHINE IN RATS - ROLE OF ENDOGENOUS PROSTAGLANDINS

  • 1 January 1981
    • journal article
    • research article
    • Vol. 16  (1) , 7-12
Abstract
Intragastric administration of aspirin (ASA) plus 0.15 M HCl to fasted rats produced typical gastric ulcers accompanied by almost complete disappearance of mucosal prostaglandins (PG). Pretreatment with various exogenous PG that were biologically inactive (e.g., 6-keto-PGF1.alpha., or PGF2.beta.) or active (PGF2 and PGI2) but used in non-antisecretory doses prevented the formation of these gastric lesions (cytoprotection). Besides PG, antisecretory compounds such as ranitidine, a new H2-receptor antagonist and probanthine were also cytoprotective, even when given in non-antisecretory doses. Mucosal generation of PG in animals treated with ASA and HCl plus ranitidine or probanthine was very low and not significantly different from those receiving only ASA and HCl. The cytoprotection is apparently not only the property of PG but also of conventional gastric antisecretory compounds, such as H2-receptor antagonists or anticholinergies. This cytoprotection can be demonstrated under conditions excluding any role of gastric secretory inhibition and in the absence of endogenous PG.