Supplementary Material for: The Impact of Obstructive Sleep Apnea and Tobacco Smoking on Endothelial Function

<b><i>Background:</i></b> Endothelial dysfunction has been recognized to occur in the context of obstructive sleep apnea (OSA) or tobacco smoking. However, the deleterious effect on vascular function with concurrence of both conditions is largely unknown. <b><i>Objective:</i></b> To investigate whether the concurrence of OSA and smoking poses an additive detriment to endothelial dysfunction. <b><i>Methods:</i></b> Chinese men without a history of chronic medical illness were invited to complete a questionnaire including smoking pack-year exposure, polysomnography and peripheral arterial tonometry (PAT) for endothelial function. Serum 8-isoprostane, advanced oxidation protein products (AOPP) and monocyte chemo-attractant protein-1 (MCP-1) were measured. <b><i>Results:</i></b> 114 men were successfully enrolled. PAT ratio, adjusted for age and body mass index, correlated inversely with overall severity of OSA: apnea-hypopnea index (AHI), r = -0.160 (p = 0.092); oxygen desaturation index, r = -0.214 (p = 0.024); duration of oxygen saturation <90%, r = -0.219 (p = 0.020); and minimum oxygen saturation, r = 0.250 (p = 0.008). The PAT ratio decreased with increasing pack-year group (p = 0.018). It was lower with concurrent smoking history and moderate-severe OSA (AHI ≥15/h) compared to having one or neither factor (p = 0.011). Serum levels of 8-isoprostane and AOPP were positively related to severity of OSA, while MCP-1 correlated with smoking quantity. Multiple linear regression analyses showed that severity of intermittent hypoxia, MCP-1 and pack-year exposure were independent predictors of PAT ratio. <b><i>Conclusion:</i></b> While OSA, in particular intermittent hypoxemia, and tobacco smoking were independent risk factors, the concurrence of moderate-severe OSA and smoking was associated with the most severe impairment in endothelial function

Molecular characterization of autonomic and neuropeptide receptors

© 1994 by Marcel Dekker, Inc. All Rights Reserved. For many years, it was believed that the control of airway function was dependent on the balance between the cholinergic (parasympathetic) and adrenergic (sympathetic) nervous systems. The cholinergic system is considered excitatory because it plays a role in maintaining airway tone and in mediating acute bronchospastic responses (Casale, 1993). The effect of acetylcholine to produce narrowing of the airways is blocked by atropine, indicating that this effect is mediated by muscarinic acetylcholine receptors (Colebatch and Halmagyi, 1963; Olsen et al., 1965). In contrast, the adrenergic system in the lung is considered inhibitory because stimulation of β-adrenergic receptors produces relaxation of bronchial smooth muscle. The beta-blockade theory of the pathogenesis of asthma from Szentivanyi (1968) proposed that asthma was related to an imbalance in the autonomic control of airway diameter due to a decrease in β-adrenergic sensitivity in bronchial smooth muscle, mucus glands, and mucosal blood vessels