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1 Biomedical Engineering, University of California, Irvine, Irvine, California, United States
2 Pediatrics, University of California, Irvine, Irvine, California, United States; General Clinical Research Center, University of California, Irvine, Irvine, California, United States
3 Medicine, University of California Irvine Medical Center, Orange, California, United States; Biomedical Engineering, University of California, Irvine, Irvine, California, United States
4 General Clinical Research Center, University of California, Irvine, Irvine, California, United States
5 Center for Statistical Consulting, University of California, Irvine, Irvine, California, United States; General Clinical Research Center, University of California, Irvine, Irvine, California, United States
6 Pediatrics, University of California @ Irvine College of Medicine, Orange, California, United States; Biomedical Engineering, University of California, Irvine, Irvine, California, United States; General Clinical Research Center, University of California, Irvine, Irvine, California, United States
7 Biomedical Engineering, University of California-Irvine, 3120 Natural Sciences II, Irvine, California, 92717-2715, United States; Chemical Engineering and Materials Science, University of California, Irvine, Irvine, California, United States
* To whom correspondence should be addressed. E-mail: scgeorge{at}uci.edu.
Exhaled nitric oxide is altered in asthmatic subjects with exercise-induced bronchoconstriction (EIB). However, the physiological interpretation of exhaled nitric oxide is limited due to its dependence on exhalation flow, and inability to distinguish completely proximal (large airway) from peripheral (small airway and alveolar) contributions. We estimated flow-independent nitric oxide exchange parameters that partition exhaled nitric oxide into proximal and peripheral contributions at baseline, post-exercise challenge, and post-bronchodilator administration in steroid naive mild-intermittent asthmatic subjects with exercise-induced bronchoconstriction (24-43 years old, n=9) and healthy controls (20-31 years old, n=9). The mean±SD maximum airway wall flux (pl.s-1) and the airway diffusing capacity (pl.s-1ppb-1)), were elevated while FEF25-75 (liters), FEV1 (%predicted), and FEV1/FVC were reduced at baseline in subjects with EIB compared to healthy controls (2050±1286, 8.4±7.3, 2.2±1.2, 75.7±18.8, 69±8.5 compared to 484±227, 3.1±1.3, 4.0±0.7, 101±9.4, and 86±3.0, respectively) whereas the steady state alveolar concentration of nitric oxide, and FVC were not different. Compared to the response of healthy controls, exercise challenge significantly reduced FEV1 (-23±15%), FEF25-75 (-37±18%), FVC (-12±12%), FEV1/FVC (-13±8%) and the maximum airway wall flux (-35±11%), relative to baseline in subjects with EIB while bronchodilator administration only increased FEV1(+20±21%), FEF25-75 (+56±41%), and FEV1/FVC (+13±9%). We conclude that mild-intermittent steroid naive asthmatic subjects with EIB have altered airway nitric oxide exchange dynamics at baseline and following exercise challenge, but these changes occur by distinct mechanisms, and are not correlated with alterations in spirometry.
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