Bronchodilation and inhibition of induced asthma by adrenergic agonists

Peyton A. Eggleston, Patsy P. Beasley

Research output: Contribution to journalArticlepeer-review

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-μg inhaled dose of the rapidly metabolized agonist, isoproterenol, induced bronchodilation of the same order as terbutaline 500 μg (1-sec 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 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 < 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.

Original languageEnglish (US)
Pages (from-to)505-510
Number of pages6
JournalClinical pharmacology and therapeutics
Volume29
Issue number4
DOIs
StatePublished - Apr 1981

ASJC Scopus subject areas

  • Pharmacology
  • Pharmacology (medical)

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