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Original Research: SLEEP MEDICINE |

Alveolar-Derived Exhaled Nitric Oxide Is Reduced in Obstructive Sleep Apnea Syndrome*

Antonio Foresi, MD, FCCP; Clementina Leone, PhD; Dario Olivieri, MD, FCCP; George Cremona, MD
Author and Funding Information

*From the Unit of Respiratory Medicine (Drs. Foresi and Leone), Sesto San Giovanni Hospital, Sesto San Giovanni; the Department of Clinical Sciences (Dr. Olivieri), Section of Respiratory Diseases, University of Parma, Parma; and the Unit of Respiratory Medicine (Dr. Cremona), San Raffaele University Hospital, Milan, Italy.

Correspondence to: George Cremona, MD, Unit of Respiratory Medicine, San Raffaele University Hospital, Via Olgettina 60, 20132 Milano, Italy; e-mail george.cremona@hsr.it



Chest. 2007;132(3):860-867. doi:10.1378/chest.06-3124
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Background: Obstructive sleep apnea syndrome (OSAS) is associated with cardiovascular diseases, in particular systemic arterial hypertension. We postulated that intermittent nocturnal hypoxia in OSAS may be associated to decreased fractional exhaled nitric oxide (FENO) levels from distal airspaces.

Methods: Multiple flow rate measurements have been used to fractionate nitric oxide (NO) from alveolar and bronchial sources in 34 patients with OSAS, in 29 healthy control subjects, and in 8 hypertensive non-OSAS patients. The effect of 2 days of treatment with nasal continuous positive airway pressure (nCPAP) on FENO was examined in 18 patients with severe OSAS.

Results: We found that the mean [± SE] concentrations of exhaled NO at a rate of 50 mL/s was 21.8 ± 1.9 parts per billion (ppb) in patients with OSAS, 25.1 ± 3.3 ppb in healthy control subjects, and 15.4 ± 1.7 ppb in hypertensive control patients. The mean fractional alveolar NO concentration (CANO) in OSAS patients was significantly lower than that in control subjects (2.96 ± 0.48 vs 5.35 ± 0.83 ppb, respectively; p < 0.05). In addition, CANO values were significantly lower in OSAS patients with systemic hypertension compared to those in normotensive OSAS patients and hypertensive patients without OSAS. The mean values of CANO significantly improved after nCPAP therapy (2.67 ± 0.41 to 4.69 ± 0.74 nL/L, respectively; p = 0.01).

Conclusions: These findings suggest that alveolar FENO, and not bronchial FENO, is impaired in patients with OSAS and that this impairment is associated with an increased risk of hypertension. NO production within the alveolar space is modified by treatment with nCPAP.

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