Generation of endogenous prostaglandins and thromboxanes in taurocholate-induced gastric mucosal lesions.

Abstract

This study demonstrates that the suppression of thromboxane biosynthesis by OKY-1581, a selective inhibitor of thromboxane biosynthesis, prevents dose-dependently taurocholate-induced gastric mucosal necrosis and enhances the cytoprotective effect of low dose of taurocholate against mucosal necrosis by large dose of this agent. In all animals treated with OKY-1581, a decrease in mucosal generation of thromboxane was accompanied by an increased production of PGs probably due to availability of greater amounts of a common substrate in a cyclooxygenase pathway. This study provides direct evidence that gastric mucosa generates thromboxanes which may be involved in the pathogenesis of taurocholate-induced gastric mucosal lesions.

• Authors: S J Konturek, T Brzozowski, T Radecki, M Dobrzańska
• Journal: Scandinavian journal of gastroenterology. Supplement (Scand J Gastroenterol Suppl) Vol. 92 Pg. 91-6 ( 1984) ISSN: 0085-5928 [Print] England
• PMID: 6377475 (Publication Type: Journal Article)

Chemical References

• Methacrylates
• Prostaglandins
• Prostaglandins E
• Thromboxanes
• Thromboxane B2
• Taurocholic Acid
• 2-methyl-3-(4-(3-pyridinylmethyl)phenyl)-2-propenoic acid
• Epoprostenol
• Thromboxane-A Synthase
• Dinoprostone
• Indomethacin

Topics

• Animals
• Dinoprostone
• Epoprostenol (biosynthesis)
• Female
• Gastric Mucosa (drug effects, metabolism, pathology)
• Indomethacin (pharmacology)
• Male
• Methacrylates (pharmacology)
• Necrosis
• Prostaglandins (biosynthesis)
• Prostaglandins E (biosynthesis)
• Rats
• Rats, Inbred Strains
• Taurocholic Acid (pharmacology)
• Thromboxane B2 (biosynthesis)
• Thromboxane-A Synthase (antagonists & inhibitors)
• Thromboxanes (biosynthesis)