INHIBITION OF PROSTAGLANDIN BIOSYNTHESIS BY NON-NARCOTIC ANALGESIC DRUGS

  • 1 January 1976
    • journal article
    • research article
    • Vol. 224  (1) , 30-42
Abstract
The existence of a relationship between inhibition of prostaglandin biosynthesis and analgesic or anti-inflammatory activity was investigated in the case of the non-narcotic analgesics glafenine, floctafenine and clometacin, in comparison to indomethacin and acetylsalicylic acid. These compounds inhibit prostaglandin biosynthesis from arachidonic acid in a guinea-pig lung homogenate as strongly as indomethacin. On its biosynthesis in rat epididymal tissue stimulated by noradrenaline [norepinephrine], glafenine equals indomethacin inhibitory potency, whereas floctafenine and clometacine are less active. Acetylsalicylic acid is the least active in both preparations. In vivo, prostaglandin biosynthesis induced in rat peritoneal fluid by injection of acetic acid is inhibited by the 5 drugs, ranked as follows: floctafenine > indomethacin > glafenine > clometacin > acetylsalicylic acid. The pharmacological profile of glafenine, floctafenine and clometacin is characterized by a relatively strong effect on acetic acid writhing and a relatively weak effect on carrageenin edema, UV erythema and adjuvant arthritis. The inhibition of prostaglandin biosynthesis seems better correlated with their analgesic activity than with their anti-inflammatory effects. Prostaglandins could play an important role in the genesis of tissulary pain in animals.