Bronchodilation and inhibition of induced asthma by adrenergic agonists

Abstract

In asthma, adrenergic agonists alleviate airflow obstruction and prevent obstructive responses to a variety of stimuli. A rapidly and a slowly metabolized agonist were compared to determine whether bronchodilation is the major mechanism by which these drugs prevent exercise-induced asthma (EIA). A 200-.mu.g inhaled dose of the rapidly metabolized agonist, isoproterenol, induced bronchodilation of the same order as terbutaline 500 .mu.g (1-s forced expiratory volume [FEV1] increased 9.5% and 10.2%). An hour after isoproterenol, FEV1 was still above baseline (P < 0.02), but EIA was only partially inhibited; the 23% fall in FEV1 was of the same order as the 32% fall after placebo (P > 0.05). One h after terbutaline, mean resting FEV1 was in the range of that after isoproterenol, but the 10% change after exercise was less than that after placebo and isoproterenol (P < 0.005). The 2 effects have different dose-response relationships, with higher doses of adrenergic agonists needed to prevent EIA than to maintain bronchodilation.