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J Appl Physiol (June 2, 2005). doi:10.1152/japplphysiol.00383.2005
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Submitted on April 5, 2005
Accepted on May 18, 2005

BROADBAND FREQUENCY DEPENDENCE OF RESPIRATORY IMPEDANCE IN RATS

Cindy Thamrin1, Peter D. Sly1, and Zoltan Hantos2*

1 Division of Clinical Sciences, Telethon Institute for Child Health Research and Centre for Child Helath Research, University of Western Australia, Perth, WA, Australia
2 Department of Medical Informatics and Engineering, University of Szeged, Szeged, Hungary

* To whom correspondence should be addressed. E-mail: hantos{at}dmi.u-szeged.hu.

Past studies in humans and other species have revealed the presence of resonances and antiresonances, i.e. minima and maxima in respiratory system impedance (Zrs), at frequencies much higher than those commonly employed in clinical applications of the forced oscillation technique (FOT). To help understand the mechanisms behind the first occurrence of antiresonance in the Zrs spectrum, the frequency response of the rat was studied using FOT at both low and high frequencies. We measured Zrs in both Wistar and PVG/c rats using the wavetube technique, with a FOT signal ranging from 2 to 900 Hz. We then compared the high-frequency parameters, i.e., the first antiresonant frequency (far,1) and the resistive part of Zrs at that frequency (Rrs(far,1)), with parameters obtained by fitting a modified constant-phase model to low-frequency Zrs spectra. far,1 was 570 ± 43(SD) Hz and 456 ± 16 Hz in Wistar and PVG/c rats, respectively, and it did not shift with respiratory gases of different densities (air, heliox and a mixture of SF6). far,1 and Rrs(far,1) were relatively independent of MCh-induced bronchoconstriction, but changed significantly with increasing transrespiratory pressures up to 20 cmH2O, in the same way as airway resistance but independently of changes to tissue parameters. These results suggest that, unlike the human situation, the first antiresonance in the rat is not primarily dependent on the acoustic dimensions of the respiratory system, and can be explained by interactions between compliances and inertances localised to the airways, but this most likely does not include airway wall compliance.







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