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Deep inspirations protect against airway closure in nonasthmatic subjects

¹Woolcock Institute of Medical Research, ²Cooperative Research Centre for Asthma, ³University of Sydney, Sydney; ⁴Department of Respiratory Medicine, Royal North Shore Hospital, St. Leonards; and ⁵Discipline of Pharmacology, Bosch Institute, University of Sydney, Sydney, Australia

Submitted 22 February 2009 ; accepted in final form 11 May 2009

The mechanism by which deep inspirations protect against increased airway responsiveness in nonasthmatic subjects is not known. The aim was to investigate the role of airway closure and airway narrowing in deep inspiration bronchoprotection. Twelve nonasthmatic and nine asthmatic subjects avoided deep inspirations (DI) for 20 min, then took five DI expired to functional residual capaciy (DI-FRC) or, on a separate day, no DI (no DI) before inhaling a single dose of methacholine. On another day, eight nonasthmatic subjects took five DI expired to residual volume (DI-RV). Peripheral airway function was measured by respiratory system reactance (Xrs), using the forced oscillation technique, and by forced vital capacity (FVC) as an index of airway closure. Respiratory system resistance (Rrs) and forced expiratory volume in 1 s (FEV₁)/FVC were measured as indexes of airway narrowing. In nonasthmatic subjects, DI-FRC reduced the response measured by FEV₁ (P = 0.019), Xrs (P = 0.02), and FVC (P = 0.0005) but not by Rrs (P = 0.15) or FEV₁/FVC (P = 0.52) compared with no DI. DI-RV had a less protective effect than DI-FRC on response measured by FEV₁ (P = 0.04) and FVC (P = 0.016). There was no difference between all protocols when the response was measured by Xrs (P = 0.20), Rrs (P = 0.88), or FEV₁/FVC (P = 0.88). DI had no effect on methacholine response in asthmatic subjects. DI protect against airway responsiveness through an effect on peripheral airways involving reduced airway closure. The protective effect of DI on FEV₁ and FVC was abolished by expiration to residual volume. We speculate that the reduced airway closure is due to reduced baseline ventilation heterogeneity and/or reduced airway surface tension.

airway hyperresponsiveness; bronchoconstriction; forced expiratory volume in 1 s; methacholine