Bronchodilator effect of deep inspiration and bronchoconstriction-triggered cough.

Noriyuki Ohkura, Masaki Fujimura, Akira Tokuda, Johsuke Hara, Akihiro Hori, Masaru Nishitsuji, Miki Abo, Nobuyuki Katayama
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引用次数: 11

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.

Abstract Image

Abstract Image

Abstract Image

深吸气与支气管收缩性咳嗽的支气管扩张作用。
背景:咳嗽变异性哮喘患者的咳嗽是由支气管收缩引起的,对支气管扩张剂治疗有反应。吸入甲胆碱引起气道狭窄后,深度吸气(DI)引起哮喘和非哮喘受试者气道扩张。本研究的目的是探讨DI的支气管扩张作用与支气管收缩引起的咳嗽之间的关系。方法:我们用部分和全流量-容量曲线测量了28名健康成人气道对甲胆碱的反应性。从全用力肺活量(MEF40)中获得残余容积以上40%的呼气流量,并以该容积作为参考容积,从部分曲线(PEF40)中确定等容积流量。在吸入高浓度的甲胆碱期间和之后,咳嗽次数为32分钟,使fev1比生理盐水后值(PC20-FEV1)下降20%或更多。在PC20-FEV1浓度下,DI对甲胆碱所致支气管收缩的支气管扩张作用用(MEF40-PEF40)/PEF40 (DI指数)的比值表示。结果:吸入乙酰胆碱PC20-FEV1浓度前后32 min咳嗽次数为39.3 +/- 29.7(平均+/- SD)/32 min。吸入乙酰胆碱PC20-FEV1浓度前后咳嗽次数与DI指数相关(r = 0.57, p = 0.0015),但与吸入乙酰胆碱PC20-FEV1或FEV1、PEF40变化无关。结论:甲胆碱致咳嗽与DI对正常受试者甲胆碱致支气管收缩的支气管扩张作用有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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