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Open Access Research

Bronchodilator effect of deep inspiration and bronchoconstriction-triggered cough

Noriyuki Ohkura*, Masaki Fujimura, Akira Tokuda, Johsuke Hara, Akihiro Hori, Masaru Nishitsuji, Miki Abo and Nobuyuki Katayama

Author Affiliations

Respiratory Medicine, Cellular Transplantation Biology, Kanazawa, University Graduate School of Medical Science, Japan

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Cough 2009, 5:9  doi:10.1186/1745-9974-5-9

Published: 20 November 2009

Abstract

Background

Cough in the patients with cough variant asthma is triggered by bronchoconstriction, which responds to bronchodilator therapy. Following airway narrowing induced by inhaled methacholine, deep inspiration (DI) causes dilation of the airways in both asthmatic and non-asthmatic subjects. The aim of the present study was to investigate the relationship between bronchodilator effect of DI and bronchoconstriction-triggered cough.

Methods

We measured airway responsiveness to methacholine using partial and full flow-volume curves in 28 healthy adults. The expiratory flow at 40% above residual volume from the full forced vital capacity (MEF40) was obtained and the volume was used as the reference volume to determine the isovolume flow from the partial curve (PEF40). Coughs were counted for 32 min during and following the inhalation of methacholine at the provocative concentration which produced a 20% fall or more in FEV1from the post-saline value (PC20-FEV1). The bronchodilator effect of DI on bronchoconstriction induced by methacholine at the PC20-FEV1 concentration was expressed as the ratio of (MEF40-PEF40)/PEF40 (DI index).

Results

The number of coughs for 32 min during and following the inhalation of PC20-FEV1 concentration of methacholine was 39.3 ± 29.7 (mean ± SD)/32 min. The number of coughs during and following the inhalation was correlated with DI index (r = 0.57, p = 0.0015), but not with PC20-FEV1 or change in FEV1 or PEF40 by inhalation of the PC20-FEV1 concentration of methacholine.

Conclusion

We found that methacholine-induced cough was associated with the bronchodilator effect of DI on methacholine induced-bronchoconstriction in normal subjects.