Airway Dysfunction in Obesity: Response to Voluntary Restoration of End Expiratory Lung Volume
Airway Dysfunction in Obesity: Response to Voluntary Restoration of End Expiratory Lung Volume
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DOI：
10.1371/journal.pone.0088015
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发表时间：
2014-02-04
期刊：
影响因子：
3.7
通讯作者：
Goldring, Roberta M.
中科院分区：
文献类型：
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作者：
Oppenheimer, Beno W.;Berger, Kenneth I.;Goldring, Roberta M.
简介：由于静息肺容量减少，肥胖患者可能发生远端肺功能异常;然而，也可能存在气道炎症、血管充血和/或伴随的内源性气道疾病。本研究的目的是1）利用肺量测定法、体积描记法和呼吸描记法描述肥胖受试者的肺功能表型;和2）评估当通过呼气末肺容积（EELV）的自主升高至预测FRC来消除质量负荷的影响时的残余异常。100名无心肺疾病且肺功能正常的非吸烟肥胖受试者接受了脉冲多普勒（IOS）检查结果：FRC和ERV降低（44 +/- 22，62 +/- 14%预测值），RV/TLC正常（29 +/- 9%）。IOS在20 Hz下显示电阻升高（R-20，4.65 +/- 1.07 cmH（2）O/L/s）;然而，电导率正常（0.14 +/- 0.04）。5-20 Hz时的电阻（R5-20，1.86 +/- 1.11 cmH（2）O/L/s）和5 Hz时的电抗（X-5，-22.70 +/- 1.44 cmH（2）O/L/s）异常。EELV升高时，IOS异常恢复正常或接近正常。尽管EELV升高（1.16 +/- 0.8 cmH（2）O/L/s），但在一些受试者中观察到R5-20的残留异常。R5-20在基线时对支气管扩张剂有反应，但在EELV升高期间无反应。结论：本研究描述了肥胖患者肺功能障碍的表型，即FRC减少伴气道狭窄、远端呼吸功能障碍和支气管扩张剂反应性。当R5-20在自主充气期间正常化时，质量负荷被认为是主要机制。相反，当R5-20中的残余异常被证实时，尽管EELV恢复到预测的FRC，除了质量负荷之外，还可以调用气道功能障碍的机制。
Introduction: Abnormality in distal lung function may occur in obesity due to reduction in resting lung volume; however, airway inflammation, vascular congestion and/or concomitant intrinsic airway disease may also be present. The goal of this study is to 1) describe the phenotype of lung function in obese subjects utilizing spirometry, plethysmography and oscillometry; and 2) evaluate residual abnormality when the effect of mass loading is removed by voluntary elevation of end expiratory lung volume (EELV) to predicted FRC.Methods: 100 non-smoking obese subjects without cardio-pulmonary disease and with normal airflow on spirometry underwent impulse oscillometry (IOS) at baseline and at the elevated EELV.Results: FRC and ERV were reduced (44 +/- 22, 62 +/- 14% predicted) with normal RV/TLC (29 +/- 9%). IOS demonstrated elevated resistance at 20 Hz (R-20, 4.65 +/- 1.07 cmH(2)O/L/s); however, specific conductance was normal (0.14 +/- 0.04). Resistance at 5-20 Hz (R5-20, 1.86 +/- 1.11 cmH(2)O/L/s) and reactance at 5 Hz (X-5, -22.70 +/- 1.44 cmH(2)O/L/s) were abnormal. During elevation of EELV, IOS abnormalities reversed to or towards normal. Residual abnormality in R5-20 was observed in some subjects despite elevation of EELV (1.16 +/- 0.8 cmH(2)O/L/s). R5-20 responded to bronchodilator at baseline but not during elevation of EELV.Conclusions: This study describes the phenotype of lung dysfunction in obesity as reduction in FRC with airway narrowing, distal respiratory dysfunction and bronchodilator responsiveness. When R5-20 normalized during voluntary inflation, mass loading was considered the predominant mechanism. In contrast, when residual abnormality in R5-20 was demonstrable despite return of EELV to predicted FRC, mechanisms for airway dysfunction in addition to mass loading could be invoked.