![]() 5, 6 Furthermore, suppression of the increased vagal tone by inhaled anticholinergic drugs leads to improvement in forced expiratory flow, 7 reduction in early morning falls in peak expiratory flow, and protection against nocturnal asthma symptoms. In fact, several studies have shown that increased vagal tone stimulates the muscarinic receptors located in the central airways leading to bronchoconstriction 4 and causing nocturnal asthma. 2, 3 Increased vagal tone occurring during apnea episodes could be a trigger for nocturnal asthma attacks in sleep apnea patients. ![]() The mechanics of this potent vagal stimulation are similar to those of the Müller maneuver, which consists of an inspiratory effort against a closed glottis. Patients with OSAS have an increased vagal tone during sleep as a consequence of partial or complete airway obstruction occurring during apneas. Clarifying the nature of the relationship between OSAS and asthma is a critical area with important therapeutic implications. The common asthmatic features that promote OSAS symptoms are nasal obstruction, a decrease in pharyngeal cross sectional area, and an increase in upper airway collapsibility. Several studies have confirmed that asthmatic patients are more prone to develop OSAS symptoms than are members of the general population. ![]() Vascular endothelial growth factor–induced airway angiogenesis, leptin-related airway changes, and OSAS-induced weight gain also may play a common mechanistic role linking both disorders. Neuromechanical reflex bronchoconstriction, gastroesophageal reflux, inflammation (local and systemic), and the indirect effect on dyspnea of OSAS-induced cardiac dysfunction have been suggested as mechanisms that lead to worsening asthma control in patients with concomitant OSAS. Recent data suggest that obstructive sleep apnea syndrome (OSAS) is an independent risk factor for asthma exacerbations. ![]()
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