EFFECT OF INHALED PGE(2) ON EXERCISE-INDUCED BRONCHOCONSTRICTION IN ASTHMATIC SUBJECTS

Previous studies have suggested that the endogenous release of inhibitory prostanoids limits the bronchoconstrictor response to repeated exercise. The aim of our study was to determine whether inhaled prostaglandin (PG)E(2) attenuates exercise-induced bronchoconstriction or methacholine airway responsiveness in asthmatic subjects. Eight subjects with mild stable asthma and exercise bronchoconstriction were studied on 4 separate days, 48 h apart. Subjects inhaled PGE(2) or placebo in a randomized, crossover, double-blind fashion, 30 min prior to an exercise challenge or a methacholine challenge. PGE(2) inhalation significantly attenuated exercise bronchoconstriction. The mean maximal %fall in FEV(1) after exercise was 26% (SEM 3.7%) after placebo, and was 9.7% (SEM 2.7%) after PGE(2) (p < 0.001). PGE(2) also significantly reduced the duration of exercise bronchoconstriction (p = 0.034). However, PGE(2) did not significantly attenuate methacholine airway responsiveness. The geometric mean methacholine provocative concentration causing a 20% fall in FEV(1) (PC20) was 0.77 (%SEM 1.48) after placebo day, and 1.41 (%SEM 2.20) after PGE(2) (p = 0.30). These results demonstrate that inhaled PGE(2) markedly attenuates exercise bronchoconstriction in asthmatic subjects and suggest that this effect is not occurring through functional antagonism of airway smooth muscle.