Bronchodilation and inhibition of induced asthma by adrenergic agonists

Peyton A. Eggleston, Patsy P. Beasley

Research output: Contribution to journalArticle

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
StatePublished - Apr 1981
Externally publishedYes

Fingerprint

Adrenergic Agonists
Isoproterenol
Asthma
Exercise-Induced Asthma
Terbutaline
Forced Expiratory Volume
Placebos
Pharmaceutical Preparations

ASJC Scopus subject areas

  • Pharmacology

Cite this

Bronchodilation and inhibition of induced asthma by adrenergic agonists. / Eggleston, Peyton A.; Beasley, Patsy P.

In: Clinical Pharmacology and Therapeutics, Vol. 29, No. 4, 04.1981, p. 505-510.

Research output: Contribution to journalArticle

Eggleston, Peyton A. ; Beasley, Patsy P. / Bronchodilation and inhibition of induced asthma by adrenergic agonists. In: Clinical Pharmacology and Therapeutics. 1981 ; Vol. 29, No. 4. pp. 505-510.
@article{f6999ea33f964464aaffc4a6c47fbe4e,
title = "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-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.",
author = "Eggleston, {Peyton A.} and Beasley, {Patsy P.}",
year = "1981",
month = "4",
language = "English (US)",
volume = "29",
pages = "505--510",
journal = "Clinical Pharmacology and Therapeutics",
issn = "0009-9236",
publisher = "Nature Publishing Group",
number = "4",

}

TY - JOUR

T1 - Bronchodilation and inhibition of induced asthma by adrenergic agonists

AU - Eggleston, Peyton A.

AU - Beasley, Patsy P.

PY - 1981/4

Y1 - 1981/4

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0019488366&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0019488366&partnerID=8YFLogxK

M3 - Article

C2 - 7471617

AN - SCOPUS:0019488366

VL - 29

SP - 505

EP - 510

JO - Clinical Pharmacology and Therapeutics

JF - Clinical Pharmacology and Therapeutics

SN - 0009-9236

IS - 4

ER -