Rapid corticosteroid effect on β2-adrenergic airway and airway vascular reactivity in patients with mild asthma

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12 Citations (Scopus)

Abstract

Background: Long-term glucocorticoid therapy has been suggested to improve airway and airway vascular smooth muscle responsiveness to inhaled β2-agonists in patients with asthma. Objective: We sought to assess whether a single dose of an inhaled glucocorticoid acutely potentiates β2-adrenergic airway and airway vascular smooth muscle reactivity in asthma. Methods: In 10 asthmatic and 10 healthy subjects, airway blood flow and FEV1 were measured before and 30 minutes after fluticasone or placebo inhalation and 15 minutes after the subsequent inhalation of racemic albuterol (0.6 mg or 1.25 mg) or (R)-albuterol (0.3 mg or 0.6 mg). Results: In healthy subjects all albuterol formulations increased airway blood flow equally after placebo or fluticasone pretreatment. In asthmatic subjects airway blood flow response was blunted after placebo and acutely restored after fluticasone pretreatment. Fluticasone pretreatment did not increase FEV1 responses to any albuterol formulation, except 0.6 mg racemic albuterol. Conclusion: A single dose of an inhaled glucocorticoid restores β2-adrenergic airway vasodilator responses in patients with mild asthma. The mechanism of this rapid glucocorticoid effect remains to be clarified.

Original languageEnglish
Pages (from-to)700-704
Number of pages5
JournalJournal of Allergy and Clinical Immunology
Volume121
Issue number3
DOIs
StatePublished - Mar 1 2008

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Albuterol
Adrenergic Agents
Blood Vessels
Adrenal Cortex Hormones
Asthma
Glucocorticoids
Placebos
Vascular Smooth Muscle
Inhalation
Healthy Volunteers
Vasodilator Agents
Fluticasone

Keywords

  • β-agonists
  • airway blood flow
  • albuterol
  • Asthma
  • corticosteroids
  • fluticasone
  • levalbuterol
  • nongenomic action

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

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title = "Rapid corticosteroid effect on β2-adrenergic airway and airway vascular reactivity in patients with mild asthma",
abstract = "Background: Long-term glucocorticoid therapy has been suggested to improve airway and airway vascular smooth muscle responsiveness to inhaled β2-agonists in patients with asthma. Objective: We sought to assess whether a single dose of an inhaled glucocorticoid acutely potentiates β2-adrenergic airway and airway vascular smooth muscle reactivity in asthma. Methods: In 10 asthmatic and 10 healthy subjects, airway blood flow and FEV1 were measured before and 30 minutes after fluticasone or placebo inhalation and 15 minutes after the subsequent inhalation of racemic albuterol (0.6 mg or 1.25 mg) or (R)-albuterol (0.3 mg or 0.6 mg). Results: In healthy subjects all albuterol formulations increased airway blood flow equally after placebo or fluticasone pretreatment. In asthmatic subjects airway blood flow response was blunted after placebo and acutely restored after fluticasone pretreatment. Fluticasone pretreatment did not increase FEV1 responses to any albuterol formulation, except 0.6 mg racemic albuterol. Conclusion: A single dose of an inhaled glucocorticoid restores β2-adrenergic airway vasodilator responses in patients with mild asthma. The mechanism of this rapid glucocorticoid effect remains to be clarified.",
keywords = "β-agonists, airway blood flow, albuterol, Asthma, corticosteroids, fluticasone, levalbuterol, nongenomic action",
author = "Eliana Mendes and Gabor Horvath and Campos, {Michael A} and Adam Wanner",
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T1 - Rapid corticosteroid effect on β2-adrenergic airway and airway vascular reactivity in patients with mild asthma

AU - Mendes, Eliana

AU - Horvath, Gabor

AU - Campos, Michael A

AU - Wanner, Adam

PY - 2008/3/1

Y1 - 2008/3/1

N2 - Background: Long-term glucocorticoid therapy has been suggested to improve airway and airway vascular smooth muscle responsiveness to inhaled β2-agonists in patients with asthma. Objective: We sought to assess whether a single dose of an inhaled glucocorticoid acutely potentiates β2-adrenergic airway and airway vascular smooth muscle reactivity in asthma. Methods: In 10 asthmatic and 10 healthy subjects, airway blood flow and FEV1 were measured before and 30 minutes after fluticasone or placebo inhalation and 15 minutes after the subsequent inhalation of racemic albuterol (0.6 mg or 1.25 mg) or (R)-albuterol (0.3 mg or 0.6 mg). Results: In healthy subjects all albuterol formulations increased airway blood flow equally after placebo or fluticasone pretreatment. In asthmatic subjects airway blood flow response was blunted after placebo and acutely restored after fluticasone pretreatment. Fluticasone pretreatment did not increase FEV1 responses to any albuterol formulation, except 0.6 mg racemic albuterol. Conclusion: A single dose of an inhaled glucocorticoid restores β2-adrenergic airway vasodilator responses in patients with mild asthma. The mechanism of this rapid glucocorticoid effect remains to be clarified.

AB - Background: Long-term glucocorticoid therapy has been suggested to improve airway and airway vascular smooth muscle responsiveness to inhaled β2-agonists in patients with asthma. Objective: We sought to assess whether a single dose of an inhaled glucocorticoid acutely potentiates β2-adrenergic airway and airway vascular smooth muscle reactivity in asthma. Methods: In 10 asthmatic and 10 healthy subjects, airway blood flow and FEV1 were measured before and 30 minutes after fluticasone or placebo inhalation and 15 minutes after the subsequent inhalation of racemic albuterol (0.6 mg or 1.25 mg) or (R)-albuterol (0.3 mg or 0.6 mg). Results: In healthy subjects all albuterol formulations increased airway blood flow equally after placebo or fluticasone pretreatment. In asthmatic subjects airway blood flow response was blunted after placebo and acutely restored after fluticasone pretreatment. Fluticasone pretreatment did not increase FEV1 responses to any albuterol formulation, except 0.6 mg racemic albuterol. Conclusion: A single dose of an inhaled glucocorticoid restores β2-adrenergic airway vasodilator responses in patients with mild asthma. The mechanism of this rapid glucocorticoid effect remains to be clarified.

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