1988American Review of Respiratory DiseaseRequires access

Inhibition of Methacholine-induced Bronchoconstriction in Patients with Chronic Obstructive Pulmonary Disease

Lee Greenspon, Beth Parrish

Open publisher page 16 citations

Abstract

Patients with COPD have increased airway responsiveness to pharmacologically induced bronchoconstriction when compared with normal healthy subjects. We questioned whether an inhaled bronchodilator such as isoproterenol would benefit patients with COPD by inhibiting inducible bronchoconstriction. Ten patients with COPD were found to be more sensitive to methacholine by inhalation bronchial challenge testing than were normal control subjects. (PD35 = 58 +/- 110 versus 238 +/- 220 cumulative dose units). Neither group as a whole demonstrated significant inhibition of methacholine-induced bronchoconstriction by prior inhalation of isoproterenol (200 micrograms at mouth). However, within the COPD group, there was a significant negative correlation between both baseline lung function and airway responsiveness (PD35-SGaw) with inhibition of methacholine-induced bronchoconstriction. (r = -0.8, p less than or equal to 0.003). This suggests that those patients with COPD and significantly reduced lung function (%FEV1 less than 50%) demonstrate airway hyperresponsiveness to a degree recorded in asthma and may benefit from therapy that inhibits airway responsiveness.

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What this paper is about

Patients with COPD have increased airway responsiveness to pharmacologically induced bronchoconstriction when compared with normal healthy subjects. We questioned whether an inhaled bronchodilator such as isoproterenol would benefit patients with COPD by inhibiting inducible bronchoconstriction. Ten patients with COPD were found to be more sensitive to methacholine by inhalation bronchial challenge testing than were normal control subjects. (PD35 = 58 +/- 110 versus 238 +/- 220 cumulative dose units). Neither group as a whole demonstrated significant inhibition of methacholine-induced bronchoconstriction by prior inhalation of isoproterenol (200 micrograms at mouth). However, within the COPD group, there was a significant negative correlation between both baseline lung function and airway responsiveness (PD35-SGaw) with inhibition of methacholine-induced bronchoconstriction. (r = -0.8, p less than or equal to 0.003). This suggests that those patients with COPD and significantly reduced lung function (%FEV1 less than 50%) demonstrate airway hyperresponsiveness to a degree recorded in asthma and may benefit from therapy that inhibits airway responsiveness.

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Available abstract

Patients with COPD have increased airway responsiveness to pharmacologically induced bronchoconstriction when compared with normal healthy subjects. We questioned whether an inhaled bronchodilator such as isoproterenol would benefit patients with COPD by inhibiting inducible bronchoconstriction. Ten patients with COPD were found to be more sensitive to methacholine by inhalation bronchial challenge testing than were normal control subjects. (PD35 = 58 +/- 110 versus 238 +/- 220 cumulative dose units). Neither group as a whole demonstrated significant inhibition of methacholine-induced bronchoconstriction by prior inhalation of isoproterenol (200 micrograms at mouth). However, within the COPD group, there was a significant negative correlation between both baseline lung function and airway responsiveness (PD35-SGaw) with inhibition of methacholine-induced bronchoconstriction. (r = -0.8, p less than or equal to 0.003). This suggests that those patients with COPD and significantly reduced lung function (%FEV1 less than 50%) demonstrate airway hyperresponsiveness to a degree recorded in asthma and may benefit from therapy that inhibits airway responsiveness.

Key concepts: Bronchoconstriction, Methacholine, Medicine, COPD, Inhalation, Asthma, Airway, Bronchodilator

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