ABSTRACT
Obstructive sleep apnea (OSA) is a prevalent disorder that is characterized by repeated episodes of upper airway obstruction during sleep (1-3). Upper airway closure results in reduction or cessation of breathing, leading to progressive hypoxemia and hypercapnia and increasing inspiratory efforts against the occluded airway. These stimuli ultimately provoke arousal from sleep, which leads to restoration of upper airway patency and resumption of breathing. An increasing body of clinical and epidemiological literature indicates that the sleep fragmentation and recurrent hypoxemia associated with OSA lead to a host of important neuropsychological, cardiovascular, respiratory control, and other disturbances, which in turn result in substantial morbidity and mortality (3-5). However, the investigation of the mechanisms by which these complications are produced has been hampered by the methodologic restrictions inherent to investigations involving humans, and by the fact that once the human condition comes to clinical attention, it has typically been present for some time. It is therefore difficult to determine which abnormalities represent a primary
factor contributing to the disorder, a secondary complication of it, or an indirectly associated comorbidity.
