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1 Department of Medicine, University of Vermont College of Medicine, Burlington, VT, USA
2 Department of Clinical Physiology, Malmo University Hospital, Lund University, Malmo, Sweden
3 Departamento de Engenharia Eletrica, Universidade do Estado de Santa Catarina, Joinville, Brazil
* To whom correspondence should be addressed. E-mail: david.kaminsky{at}uvm.edu.
To more precisely measure the mechanical properties of the lung periphery in asthma, we have developed a forced oscillation technique that applies a broad-band flow signal through a wedged bronchoscope. We interpreted the data from 4 healthy and 8 mild asthmatic subjects in terms of an anatomically accurate computer model of the wedged segment. There was substantial overlap in impedance between the two groups, with resistance (R) showing minimal frequency dependence and elastance (E) showing both positive and negative frequency dependence across subjects. Following directly instilled methacholine, R rose in both groups, but compared to healthy subjects, the asthmatic subjects displayed upward, parallel shifts in their dose-response curves. The baseline frequency-response patterns of E were enhanced following methacholine. Frequency-dependencies of R and E were well reproduced in 2 normal subjects by a computational model that employed rigid airways connected to constant-phase tissue units, but were better reproduced in the other 2 normals and 3 asthmatics when the model employed heterogeneous, peripheral airway narrowing and compliant airways. To capture the frequency-dependencies of R and E in the remaining 5 asthmatics, the model was modified by increasing airway wall stiffness. These results indicate that the lung periphery of mild asthmatic subjects is not well distinguished from that of healthy subjects by measurement of mechanical impedance at baseline, but group differences are seen following challenge with methacholine. Modeling of the response suggests that variable contributions of airway narrowing and wall compliance are operative in determining overall mechanical impedance of the lung periphery in humans with asthma, likely reflecting the functional consequences of airway inflammation and remodeling.
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