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Original Research: Asthma |

Mechanisms of Decrease in Fractional Exhaled Nitric Oxide During Acute BronchoconstrictionExhaled Nitric Oxide and Bronchoconstriction

Ilaria Cattoni, MD; Gabriella Guarnieri, MD; Alessandro Tosetto, MD; Paola Mason, MD; Maria C. Scarpa, PhD; Marina Saetta, MD, FCCP; Piero Maestrelli, MD
Author and Funding Information

From the Department of Cardiologic, Thoracic and Vascular Sciences, University of Padova, Padova, Italy.

Correspondence to: Piero Maestrelli, Dipartimento di Scienze Cardiologiche, Toraciche e Vascolari, Università degli Studi di Padova, via Giustiniani 2, 35128 Padova, Italy; e-mail: piero.maestrelli@unipd.it


Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.

Funding/Support: This work was supported by grants from the Italian Ministry of Education, University and Research; the University of Padova; and Associazione Ricerca Cura Asma (ARCA), Padova, Italy.


Chest. 2013;143(5):1269-1276. doi:10.1378/chest.12-1374
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Background:  Fractional exhaled nitric oxide measured at expiratory flow of 50 mL/s (Feno50), a biomarker of airway inflammation, is affected by changes in airway caliber. Whether a lower Feno50 level during bronchoconstriction is only an artifact due to the strong flow dependence of this parameter is controversial.

Methods:  We aimed to evaluate the dynamics of airway and alveolar nitric oxide (NO) during acute bronchoconstriction induced by methacholine. Exhaled NO was measured at expiratory flows of 10, 50, 100, 150, and 250 mL/s before and after metacholine in 26 responders to methacholine and 37 nonresponders. Flow-independent parameters (airway wall NO flux, airway NO diffusing capacity, airway wall NO concentration, alveolar NO concentration) were calculated using a two-compartment model, and correction for NO axial back diffusion was applied.

Results:  Bronchoconstriction in responders was associated with a decrease in Feno50 (−28%, P < .0001), in airway wall NO flux (−34%, P < .0001), and in airway NO diffusing capacity (−15%, P < .05). In contrast, alveolar NO concentration was not affected by bronchoconstriction. Postmethacholine changes in Feno50 were more strictly related to the ventilation distribution, assessed by single-breath carbon monoxide uptake, than to larger airways caliber, assessed by FEV1. When bronchoconstriction was reversed by salbutamol, airway wall NO flux and airway NO diffusing capacity returned to values comparable to those measured premethacholine.

Conclusions:  The changes in airway caliber induced by noninflammatory stimuli alter NO transport in the lung. The changes in NO dynamics are limited to conductive airways and are characterized by a reduction of NO flow to luminal space.

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