Obstructive sleep apnea is a common disease that may affect as many as 2% of women and 4% of men. Obesity is a major risk factor for its development. The disease results from partial or complete cessation of airflow during sleep secondary to collapse of the upper airway. This results in recurrent arousal, nocturnal oxyhemoglobin desaturation, arrhythmias, daytime hypersomnolence and possible sequelae including hypertension and cardiovascular disease. The etiology of the collapse of the upper airway is not known. Some investigators believe that there is an anatomic defect in the upper airway, others believe that there is a neural reflex defect. This proposal will examine neural reflex responses that may predispose the upper airway to collapse. The hypothesis is that increased collapsibility of the upper airway in patients with OSA is primarily secondary to a defect in neural reflex control of the upper airway.
In Specific Aim #1, the reflex responses of the upper airway to changes in nasal pressure will be measured in a cross- sectional analysis in a group of sleeping, weight-matched humans with and without obstructive sleep apnea.
In Specific Aim #2, the effects of hypercapnia on upper airway collapsibility will be measured in the same group of patients. This proposal will elucidate the role of neural reflexes in the pathogenesis of obstructive sleep apnea.
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