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: 3.09). 04/2011; 105(4):630-6. DOI: 10.1016/j.rmed.2010.12.004
Source: PubMed


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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    ABSTRACT: To assess distal/alveolar inflammation in patients with suggestive symptoms of obstructive sleep apnoea (OSA) using exhaled nitric oxide (NO) measured by two-compartment model (2-CM) after correction for axial NO back-diffusion (trumpet model). Ninety five patients suspected for OSA prospectively underwent pulmonary function test, overnight polysomnography (PSG), and exhaled NO measurement. Patients with apnoea-hypopnoea index (AHI) <5/hour were included in non-OSA group. Exhaled NO was repeatedly measured after PSG in 21 OSA patients and 8 non-OSA subjects. Alveolar NO concentration (CANO) was significantly higher in OSA patients (n=71; 4.07±1.7ppb) as compared with non-OSA subjects (n=24; 2.24±1.06ppb; p<0.0001) whilst maximal bronchial NO flux (J'awNO) and fractional exhaled NO (FENO) did not differ between the two groups. CANO was strongly associated to AHI (r=0.701; p<0.0001) and to recording time with SaO2<90% (ST-90%; r=0.659; p<0.0001) in OSA patients but not in non-OSA persons. The area under ROC curve for screening patients with OSA and significant nocturnal oxygen desaturation (ST-90%>1%) was 0.865±0.036 (95% IC, 0.793-0.937; p<0.0001). CANO at 4.5 ppb could detect these patients with specificity of 94% and sensitivity of 46%. Increase of CANO measured after PSG was significantly related to oxygen desaturation index (ST-90%) in OSA patients. Increased alveolar NO concentration was related to the severity of nocturnal oxygen desaturation in patients with OSA, linking the distal airway inflammation to intermittent hypoxia. (250 words). Copyright © 2015. Published by Elsevier Inc.
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    ABSTRACT: Chronic cough is defined as cough lasting more than 2 months. Common causes for chronic cough in nonsmokers with normal chest radiographs and pulmonary functions include gastroesophageal reflux disease (GERD), cough-variant asthma (CVA), and upper airway cough syndrome (UACS). Current guidelines recommend diagnosing the etiology of chronic cough based upon the results of therapy for suspected GERD, CVA, and UACS. Despite following current recommendations for diagnosis and treatment, the cause for a significant proportion of chronic cough remains unexplained.Recent reports indicate the resolution of chronic cough following treatment of concomitantly diagnosed obstructive sleep apnea (OSA). Whether this represents a co-occurrence of two commonly prevalent disorders or a pathophysiologic relationship between OSA and cough remains unknown. This review offers insights into a pathophysiologic link between OSA and the commonly purported etiologies for cough, namely, GERD, UACS, and CVA. In addition, evidence for a relationship between airway inflammation that can trigger or perpetuate cough and OSA is discussed. This review explores mechanisms by which nocturnal continuous positive airway therapy resolves cough by improving underlying airway inflammation secondary to OSA and impacts upon GERD, CVA, and UACS.
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    ABSTRACT: Brachycephalic dogs (BD) are prone to congenital upper airway obstruction (brachycephalic syndrome, BS). In humans suffering from sleep apnea, upper airway obstruction is known to cause hypertension. There is no information regarding the influence of BS in dogs on cardiorespiratory physiology. BD are prone to lower P(a) O(2), higher P(a) CO (2), and hypertension compared with meso- or dolicocephalic dogs (MDD). Eleven BD and 11 MDD. After a questionnaire was completed by the owner, a physical examination was performed. Height and thoracic circumferences were measured. Arterial blood gases, electrolyte concentrations, and packed cell volume (PCV) were measured. Systolic (SAP), mean (MAP), and diastolic (DAP) arterial blood pressure recordings were performed. A total of 7 French and 4 English bulldogs met the inclusion criteria. The control group consisted in 6 Beagles, 2 mixed breed dogs, 1 Staffordshire Bull Terrier, 1 Parson Russell Terrier, and 1 Australian Cattle Dog. Statistically, BD had lower P(a) O(2), higher P(a) CO2, and higher PCV when compared with controls (86.2 ± 15.9 versus 100.2 ± 12.6 mmHg, P = .017; 36.3 ± 4.6 versus 32.7 ± 2.6 mmHg, P = .019; 48.2 ± 3.5 versus 44.2 ± 5.4%, P = .026, respectively). Also, they had significantly higher SAP (177.6 ± 25.0 versus 153.5 ± 21.7 mmHg, P = .013), MAP (123.3 ± 17.1 versus 108.3 ± 12.2 mmHg, P = .014), and DAP (95.3 ± 19.2 versus 83.0 ± 11.5 mmHg, P = .042). BD with a P(a) CO (2) >35 mmHg were significantly older than those with a P(a) CO (2) ≤35 mmHg (58 ± 16 and 30 ± 11 months, P = .004). Results of this study suggest that some BD are prone to lower P(a) O(2), higher P(a) CO (2), and hypertension when compared with MDD. Age may be a contributing factor.
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