Potent and selective effects of suprofen on uterine prostaglandin synthesis.
Suprofen is a non-narcotic, peripheral analgesic that exhibits potent prostaglandin (PG) synthesis inhibitory activities in a variety of subcellular tissue preparations and in vivo. The results of the present study show suprofen to be significantly more potent than either ibuprofen (6-fold) or aspirin (1000-fold) as an inhibitor of PG production by cell-free preparations of guinea pig uteri. It is selectively more potent against the production of PGF2 alpha and PGE2 than against the formation of 6-keto PGF1 alpha, the stable metabolite of prostacyclin. Suprofen is markedly more potent inhibiting the conversion of arachidonic acid to PGF2 alpha than is ibuprofen (30 times) or aspirin (1250 times). Taken together with the important role PGF2 alpha plays in the etiology of dysmenorrhea and the observation (Hahn et al., 1982) that suprofen is more potent and effective than a number of other PG synthesis inhibitors, including ibuprofen and aspirin, at reducing in vivo guinea pig uterine contractions induced by arachidonic acid, the results of the present study suggest a mechanism to support the clinical findings that suprofen is a very effective treatment for the signs and symptoms of dysmenorrhea.
D000818:Animals; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism; D004412:Dysmenorrhea / Q000188:drug therapy / Q000209:etiology; D005260:Female; D006168:Guinea Pigs; D007052:Ibuprofen / Q000494:pharmacology; D010666:Phenylpropionates / Q000494:pharmacology*; D011453:Prostaglandins / Q000096:biosynthesis*; D013496:Suprofen / Q000494:pharmacology* / Q000627:therapeutic use; D014599:Uterus / Q000187:drug effects / Q000378:metabolism*
D001095:Arachidonic Acids; D010666:Phenylpropionates; D011453:Prostaglandins; D016718:Arachidonic Acid; D013496:Suprofen; D007052:Ibuprofen