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1 Department of Biomedical Engineering, University of California, Irvine, Irvine, CA, USA
2 Department of Biomedical Engineering, University of California, Irvine, Irvine, CA, USA; Department of Chemical Engineering and Materials Science, University of California, Irvine, Irvine, CA, USA
3 General Clinical Research Center, University of California, Irvine, Irvine, CA, USA
4 Department of Pediatrics, University of California, Irvine, Irvine, CA, USA; General Clinical Research Center, University of California, Irvine, Irvine, CA, USA
* To whom correspondence should be addressed. E-mail: scgeorge{at}uci.edu.
Exhaled nitric oxide (NO) is a potential non-invasive index of lung inflammation, and is thought to arise from the alveolar and airway regions of the lungs. A two-compartment model has been used to describe NO exchange; however, the model neglects axial diffusion of NO in the gas phase, and recent theoretical studies suggest this may introduce significant error. We used heliox (80% helium, 20% oxygen) as the insufflating gas to probe the impact of axial diffusion (molecular diffusivity of NO is increased 2.3-fold relative to air) in healthy adults (21-38 year-old, n=9). Heliox decreased the plateau concentration of exhaled NO by 45% (exhalation flow rate of 50 ml/s). In addition, the total mass of NO exhaled in phase I and II following a 20-second breathhold was reduced by 36%. A single path trumpet model which considers axial diffusion predicts a 50% increase in the maximum airway flux of NO (J'awNO), and a near-zero alveolar concentration (CANO) and source. Furthermore, when NO elimination is plotted versus constant exhalation flow rate (range 50-500 ml/s), the slope has been previously interpreted as a non-zero CANO (range 1-5 ppb); however, the trumpet model predicts a positive slope of 0.4-2.1 ppb despite a zero CANO due to a diminishing impact of axial diffusion as flow rate increases. We conclude that axial diffusion leads to a significant back diffusion of NO from the airways to the alveolar region which significantly impacts the partitioning of airway and alveolar contributions to exhaled NO.
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