Rapid corticosteroid effect on beta(2)-adrenergic airway and airway vascular reactivity in patients with mild asthma.

Abstract

Long-term glucocorticoid therapy has been suggested to improve airway and airway vascular smooth muscle responsiveness to inhaled beta(2)-agonists in patients with asthma. We sought to assess whether a single dose of an inhaled glucocorticoid acutely potentiates beta(2)-adrenergic airway and airway vascular smooth muscle reactivity in asthma. In 10 asthmatic and 10 healthy subjects, airway blood flow and FEV(1) 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). 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 FEV(1) responses to any albuterol formulation, except 0.6 mg racemic albuterol. A single dose of an inhaled glucocorticoid restores beta(2)-adrenergic airway vasodilator responses in patients with mild asthma. The mechanism of this rapid glucocorticoid effect remains to be clarified.