Abstract
To the Editor: Although antiinflammatory corticosteroids are invaluable in the treatment of asthma, the nature of their antiasthmatic action remains obscure. Several possible biochemical mechanisms have been postulated, mainly from experiments with nonpulmonary tissues.1 More recently, experiments with guinea-pig lung have demonstrated that corticosteroids exert an inhibitory effect on phospholipase A2, an enzyme that liberates arachidonic acid from phospholipids.2 Since the leukotrienes (the biologically active moieties in slow-reacting substance of anaphylaxis [SRS-A]) are metabolites of arachidonic acid,3 the experiments presented below were performed to determine whether corticosteroids could inhibit the release of leukotrienes from human lung in . . .