Airway and alveolar nitric oxide measurements in obstructive sleep apnea syndrome

Sleep Laboratory, Respiratory Medicine Department, Hospital de la Santa Creu i Sant Pau, Mas Casanovas, 90, Barcelona 08025, Spain.
Respiratory medicine (Impact Factor: 2.92). 04/2011; 105(4):630-6. DOI: 10.1016/j.rmed.2010.12.004
Source: PubMed

ABSTRACT The process of intermittent hypoxia-reoxygenation produces airway inflammation and endothelial dysfunction that favors the development of cardiovascular disorders in obstructive sleep apnea syndrome (OSAS). Nitric oxide (NO) is an important mediator in airway inflammation and the regulation of endothelium-dependent vasodilation.
This study compared airway NO (FE(NO)) and alveolar NO (CA(NO)) measurements in exhaled breath in 30 OSAS patients to those of 30 healthy (non-OSAS) individuals and determined the relationship between NO levels and OSAS severity. Additionally, NO measurements were analyzed after 3 months of CPAP treatment.
The mean (±SD) FE(NO) level in the OSAS group (27.2 ± 18 ppb) was higher than in the healthy non-OSAS group (p = 0.006). The mean CA(NO) level was 1.65 ± 0.90 ppb, lower than in the non-OSAS group (p = 0.001). A significant correlation was found between FE(NO) and CA(NO) levels and the apnea-hypopnea index (AHI) in the OSAS group (r = 0.8, p < 0.05; r = -0.9, p = 0.01, respectively). FE(NO) levels decreased and CA(NO) levels increased significantly after CPAP treatment.
Severe OSAS patients have higher FE(NO) and lower CA(NO) levels and these are restored to normal after CPAP treatment, reflecting the correction of local upper airway inflammation and endothelial dysfunction present in OSAS patients. Exhaled breath techniques can be useful to identify airway inflammation and endothelial dysfunction in severe OSAS patients.

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    • "Using this simplified model, two studies reported a decrease of CANO in patients with OSA [10] [15] suggesting endothelial dysfunction that might be linked to systemic hypertension [10]. We hypothesised that in patients with advanced OSA and vascular diseases, distal/alveolar NO production might decrease [10] [15] but in patients with moderate OSA and associated lung inflammation , CANO might increase as observed in patients with systemic sclerosis [6]. It is recently suggested that taking into account NO axial backdiffusion , related to the trumpet shape of the cross-sectional area of the tracheal tree [18], can better characterise the proximal and distal exhaled NO origins in healthy subjects [19] and SSc patients [20]. "
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