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* From the Department of Medicine, Vermont Lung Center, University of Vermont College of Medicine, Burlington, VT.
Correspondence to: David A. Kaminsky, MD, Associate Professor of Medicine, Pulmonary Disease and Critical Care Medicine, University of Vermont College of Medicine, Given C-317, Burlington, VT 05405; e-mail: dkaminsk{at}zoo.uvm.edu
Previously, we1 have shown that peripheral resistance rises more in asthmatic subjects than in nonasthmatic subjects following direct stimulation with cool, dry air. To gain further insight into this response, we measured the input impedance (Z) of the lung periphery in response to methacholine by applying forced oscillations through a wedged bronchoscope in asthmatic and nonasthmatic subjects.
We used a computer-controlled piston pump (flexiVent; SCIREQ; Montreal, QU, Canada) to deliver a broad-band (ie, 0.5 to 20 Hz) oscillatory flow through the wedged bronchoscope during 8 s of apnea at functional residual capacity. Pressure at the tip of the bronchoscope and flow data were used to calculate Z. Z was measured at baseline, following escalating doses of methacholine, following three deep lung inflations (DIs), and, finally, following albuterol administration.
At baseline, the real part of Z (R) was elevated in the asthmatic subjects (two subjects) compared to the non-asthmatic subjects (three subjects). Methacholine induced an increase in R at all frequencies in both groups, but the responsiveness of the asthmatic subjects was more than two orders of magnitude greater than that of the nonasthmatic subjects. At higher doses of methacholine, R increased most in the low-frequency range, suggesting a predominantly tissue response. Following three DIs, the low-frequency R dropped more than its higher frequency component, implying a substantial tissue effect of DI. Albuterol brought R back toward baseline at all frequencies.
These preliminary data suggest the following: (1) the lung periphery of asthmatic subjects is hyperresponsive to methacholine compared to that of nonasthmatic subjects; (2) the hyperresponsiveness involves both airway and tissue compartments; and (3) the effects of DI following bronchoconstriction occur to a significant extent in the lung periphery.
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This research was supported by National Institutes of Health grants P20RR15557 and HL56638, and by the Whitaker Foundation.
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