强迫振荡技术测定哮喘患者和健康人的气道扩张性
2007/06/27
一般认为哮喘患者存在的气道扩张力的下降可能与气道弹性回缩力及支气管平滑肌张力的改变有关。Brown等为了验证这一假说，通过采用强迫振荡技术测定哮喘和正常人的肺的弹性回缩力和支气管肌张力来观察两者在气道扩张力中的作用。 并观察支气管扩张剂使用前后的气道扩张力的改变。得到的主要结果为 哮喘患者基线 FEV1 (p=0.0003)与传导力均较正常人低 (p=0.002)。在75%TLC以上的气道扩张力低于正常人(p<0.0001)，但低于 75%TLC时两者无区别。支气管扩张剂尽管可以增加哮喘患者的FEV1 (p=0.0002) 和传导力(p<0.0001)，但对气道扩张力无明显影响。它对健康对照组的传导力也有一定的提高。使用支气管扩张剂后，哮喘患者较正常人的肺弹性回缩力明显下降，压力－传导斜率也有所下降，但在压力－容积曲线与气道扩张力间并无相关性。通过这个研究，作者揭示了虽然强迫振荡法测定的气道扩张力在哮喘患者中较正常人明显下降，但与肺的弹性回缩力并无明确相关，而支气管扩张剂并不能改变这一生理变化。气道重构仍可能是哮喘发病中气道扩张力的最重要的原因。
（汪慧英 浙江大学医学院附属二院呼吸内科 310008 摘译）
Published ahead of print on April 26, 2007
Am. J. Respir. Crit. Care Med. 2007, doi:10.1164/rccm.200609-1317OC
Am. J. Respir. Crit. Care Med. 2007, doi:10.1164/rccm.200609-1317OC
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Submitted on September 14, 2006
Accepted on April 26, 2007
Accepted on April 26, 2007
Airway Distensibility in Asthmatic and Healthy Adults Measured by Forced Oscillation Technique
Nathan J Brown1*, Cheryl M Salome1, Norbert Berend1, C. William Thorpe2, and Gregory G King1
1 The Woolcock Institute of Medical Research, Camperdown, NSW, Australia; Department of Medicine, The University of Sydney, Sydney, NSW, Australia; The Cooperative Research Centre for Asthma, Sydney, Australia, 2 The Cooperative Research Centre for Asthma, Sydney, Australia; Bioengineering Institute, The University of Auckland, Auckland, New Zealand
* To whom correspondence should be addressed. E-mail: njb@woolcock.org.au.
Rationale: Reduced airway distensibility in asthmatics compared with controls may be related to differences in lung elastic recoil and bronchomotor tone. Objectives: To examine the contribution of lung elastic recoil and bronchomotor tone to airway distensibility.
Methods: We compared airway distensibility in 18 asthmatics with 19 controls before and after bronchodilator and, in a subgroup of 7 asthmatics and 8 controls, correlated distensibility with pressure-volume parameters.
Measurements: Distensibility was measured, using forced oscillation technique, as the linear slope of conductance vs volume between TLC and 75%TLC and between 75%TLC and FRC. Transpulmonary pressure was recorded concurrently with distensibility, using an esophageal balloon. Pressure-conductance data were described using linear regressions and pressure-volume data were described using exponential equations.
Main Results: Asthmatics had lower baseline FEV1 (p=0.0003) and conductance (p=0.002) than controls. Distensibility above 75%TLC was less in asthmatics than controls (p<0.0001) but there was no difference below 75%TLC. Bronchodilator did not alter distensibility despite increases in FEV1 (p=0.0002) and conductance (p<0.0001) in asthmatics, and conductance (p=0.0004) in controls. After bronchodilator, asthmatics had reduced lung elastic recoil compared with controls (p=0.03) and a reduced pressure- conductance slope (p=0.01) but there were no correlations between pressure-volume characteristics and airway distensibility.
Conclusions: Airway distensibility measured by FOT is reduced in asthmatics compared with non-asthmatics, is not related to lung elastic recoil and is unchanged by bronchodilator. Airway wall remodeling remains the most likely cause of reduced airway distensibility in asthma.
