Study into the mechanism of acetylsalicylic acid-induced bronchoconstriction.
In order to elucidate the mechanism of the acetylsalicylic acid-induced bronchoconstrictor responses which have been observed in asthmatic patients, experiments were done in cats, anesthetized by chloralose, vagotomized, and completely relaxed by infusion of suxamethonium. In about half of the experiments, the sensitivity of the bronchi to 5-hydroxytryptamine (5-HT) was considerably enhanced after the administration of 5--6 mg/kg acetylsalicylic acid, a dose which had previously been shown to suppress prostaglandin (PG) biosynthesis in the bronchi of the cat completely. No further increase in sensitivity to 5-HT occurred when higher doses of the drug were given. Immediate bronchoconstrictor reactions to the injection of acetylsalicylic acid were rare, in most instances the rise in sensitivity developed slowly during a period of about 30 min. The results are consistent with the assumption that PGE2 displays an antagonistic effect to the mediators of asthmatic bronchoconstriction or to their liberation and that inhibition of PG synthesis by acetylsalicylic acid or related drugs eliminate this function and may thus give rise to bronchospasm.
D000818:Animals; D001095:Arachidonic Acids / Q000494:pharmacology; D001241:Aspirin / Q000008:administration & dosage / Q000494:pharmacology*; D001980:Bronchi / Q000187:drug effects*; D002415:Cats; D003251:Constriction, Pathologic / Q000139:chemically induced; D005260:Female; D008297:Male; D011433:Propranolol / Q000494:pharmacology; D011458:Prostaglandins E / Q000096:biosynthesis; D011460:Prostaglandins F / Q000096:biosynthesis; D011943:Receptors, Adrenergic, beta / Q000187:drug effects; D012701:Serotonin / Q000494:pharmacology
D001095:Arachidonic Acids; D011458:Prostaglandins E; D011460:Prostaglandins F; D011943:Receptors, Adrenergic, beta; D012701:Serotonin; D011433:Propranolol; D001241:Aspirin