The production of prostacyclin (PGI2) and thromboxane A2 (TXA2) was studied in an indometacin-induced ulcer model in rats. The specific activities of prostacyclin synthetase and thromboxane synthetase as well as the tissue content of these prostaglandins were determined. The anti-ulcer effect of cimetidine and a novel agent, i.e. 1,6-dimethyl-4-oxo-1,6,7,8,9,9a-hexahydro-4H-pyrido(1,1-a)-pyrimidine-3- carboxamide (Chinoin-127) was compared in this respect. The indometacin treatment shifted the balance of TXA2/PGI2 to the formation of TXA2, and the anti-ulcer agents repaired it. The role of this balance in cytoprotection is discussed.
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