A model of obstructive sleep apnea in normal humans - Role of the upper airway

We determined whether upper airway obstruction in normal individuals with i ntact reflexes could produce the syndrome of obstructive sleep apnea. Upper airway obstruction was produced in 12 normal individuals by lowering nasal pressure to -10 cm H2O during sleep. Full night polysomnography was perfor med during two consecutive nights of sleep with subatmospheric nasal pressu re and compared with control nights before and after the negative pressure nights. We found that the application of negative pressure was associated w ith the development of recurrent obstructive apneas (non-REM-disordered bre athing rate, 32.6 +/- 34.8 and 37.8 +/- 29.1 events/h during each of two ne gative pressure nights; p < 0.001) that were associated with oxyhemoglobin desaturation, arousals from sleep, and alterations in sleep stage distribut ion. Moreover, the median daytime sleep latency after two nights of sleep w ith subatmospheric pressure fell from 6.9 +/- 1.1 to 3.4 +/- 0.6 min, and r ose significantly again to 8.1 +/- 1.5 min (p < 0.03) after the control nig ht following subatmospheric pressure nights. Our findings suggest that a de crease in the pharyngeal transmural pressure alone is a sufficient conditio n for the production of the sleep apnea syndrome in normal individuals.