Am. J. Respir. Crit. Care Med., Volume 161, Number 6, June 2000, 1979-1984

A Model of Obstructive Sleep Apnea in Normal Humans
Role of the Upper Airway

EARL D. KING, CHRISTOPHER P. O'DONNELL, PHILIP L. SMITH, and ALAN R. SCHWARTZ

Johns Hopkins Sleep Disorders Center, Division of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland

We determined whether upper airway obstruction in normal individuals with intact 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 performed during two consecutive nights of sleep with subatmospheric nasal pressure and compared with control nights before and after the negative pressure nights. We found that the application of negative pressure was associated with the development of recurrent obstructive apneas (non-REM-disordered breathing rate, 32.6 ± 34.8 and 37.8 ± 29.1 events/h during each of two negative pressure nights; p < 0.001) that were associated with oxyhemoglobin desaturation, arousals from sleep, and alterations in sleep stage distribution. Moreover, the median daytime sleep latency after two nights of sleep with subatmospheric pressure fell from 6.9 ± 1.1 to 3.4 ± 0.6 min, and rose significantly again to 8.1 ± 1.5 min (p < 0.03) after the control night following subatmospheric pressure nights. Our findings suggest that a decrease in the pharyngeal transmural pressure alone is a sufficient condition for the production of the sleep apnea syndrome in normal individuals.

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