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Bronchodilation and inhibition of induced asthma by adrenergic agonists
Author(s) -
Eggleston Peyton A,
Beasley Patsy P
Publication year - 1981
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1038/clpt.1981.70
Subject(s) - bronchodilation , terbutaline , agonist , medicine , placebo , bronchodilator , bronchodilator agents , adrenergic , asthma , isoprenaline , pharmacology , anesthesia , receptor , stimulation , alternative medicine , pathology
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‐µg inhaled dose of the rapidly metabolized agonist, isoproterenol, induced bronchodilation of the same order as terbutaline 500 µg (I‐sec forced expiratory volume [FEV 1 ] increased 9.5% and 10.2%). An hour after isoproterenol, FEV 1 was still above baseline (p < 0.02), but EIA was only partially inhibited; the 23% fall in FEV 1 was of the same order as the 32% fall after placebo (p > 0.05). One hour after terbutaline, mean resting FEV 1 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). 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. Clinical Pharmacology and Therapeutics (1981) 29, 505–510; doi: 10.1038/clpt.1981.70