Chapman David G, Berend Norbert, King Gregory G, McParland Brent E, Salome Cheryl M
Woolcock Institute of Medical Research, Cooperative REsearch Centre for Asthma, University of Sydney, P.O. Box M77 Missenden Rd, Sydney, NSW 2050, Australia.
J Appl Physiol (1985). 2009 Aug;107(2):564-9. doi: 10.1152/japplphysiol.00202.2009. Epub 2009 May 14.
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.
深吸气对非哮喘受试者气道反应性增加具有保护作用的机制尚不清楚。本研究旨在探讨气道关闭和气道狭窄在深吸气支气管保护中的作用。12名非哮喘受试者和9名哮喘受试者避免深吸气20分钟,然后吸入单剂量的乙酰甲胆碱前,进行5次深吸气至功能残气量(DI-FRC),或者在另一天,不进行深吸气(无DI)。在另一天,8名非哮喘受试者进行5次深吸气至残气量(DI-RV)。采用强迫振荡技术通过呼吸系统电抗(Xrs)测量外周气道功能,并以用力肺活量(FVC)作为气道关闭的指标。测量呼吸系统阻力(Rrs)和第1秒用力呼气量(FEV1)/FVC作为气道狭窄的指标。在非哮喘受试者中,与无DI相比,DI-FRC降低了FEV1(P = 0.019)、Xrs(P = 0.02)和FVC(P = 0.0005)测量的反应,但Rrs(P = 0.15)或FEV1/FVC(P = 0.52)没有降低。DI-RV对FEV1(P = 0.04)和FVC(P = 0.016)测量的反应的保护作用小于DI-FRC。当通过Xrs(P = 0.20)、Rrs(P = 0.88)或FEV1/FVC(P = 0.88)测量反应时,所有方案之间没有差异。DI对哮喘受试者的乙酰甲胆碱反应没有影响。深吸气通过对外周气道的作用,包括减少气道关闭,来预防气道反应性。深吸气对FEV1和FVC的保护作用在呼气至残气量时消失。我们推测气道关闭减少是由于基线通气异质性降低和/或气道表面张力降低。