Site of analgesic action of zomepirac sodium, a potent non-narcotic analgesic in experimental animals.

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Abstract
Zomepirac sodium inhibited the reflex hypertension caused by an injection of bradykinin into the splenic artery of anesthetized dogs, but not that by injection of bradykinin plus PGE1 [prostaglandin E1]. In the rat acetic acid writhing test, the potency ratio of i.p. (ED50 = 0.41 .mu.g/kg) to i.v. (ED50 = 33.5 .mu.g/kg) anti-writhing activity of zomepirac sodium was 79.2 (37.1-173), though the ratio of codeine phosphate (373 .mu.g/kg, i.p., 352 .mu.g/kg, i.v.) was 0.934. When equipotent doses of zomepirac sodium were administered to rats receiving i.p. acetic acid, the plasma zomepirac level after i.v. administration was more than 200 times that after i.p. administration, while the peritoneal exudate zomepirac contents were nearly equal after administration by both routes. Zomepirac sodium (5 .mu.g/kg) did not produce significant anti-writhing activity after intracerebroventricular administration. Zomepirac sodium apparently produced analgesic action through a strong blockade of the hyperalgesia in the peripheral system.