Bronchodilation and inhibition of induced asthma by adrenergic agonists.
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-microgram inhaled dose of the rapidly metabolized agonist, isoproterenol, induced bronchodilation of the same order as terbutaline 500 microgram (1-sec forced expiratory volume [FEV1] increased 9.5% and 10.2%). An hour after isoproterenol, FEV1 was still above baseline (p less than 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 greater than 0.05). One hour 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 less than 0.005). Our findings suggest that the two effects have different dose-response relationships, with higher doses of adrenergic agonists needed to prevent EIA than to maintain bronchodilation.
D000293:Adolescent; D000328:Adult; D001249:Asthma / Q000188:drug therapy*; D001250:Asthma, Exercise-Induced / Q000188:drug therapy*; D001993:Bronchodilator Agents; D005541:Forced Expiratory Volume; D006801:Humans; D007545:Isoproterenol / Q000494:pharmacology*; D008450:Maximal Midexpiratory Flow Rate; D013726:Terbutaline / Q000494:pharmacology*
D001993:Bronchodilator Agents; D007545:Isoproterenol; D013726:Terbutaline