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Am J Respir Crit Care Med. 1998 Apr;157(4 Pt 1):1051-7.

The hypotonic upper airway in obstructive sleep apnea: role of structures and neuromuscular activity.

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1
Johns Hopkins Sleep Disorders Center, Division of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21224, USA.

Abstract

The structural properties of the upper airway determine its collapsibility during periods of muscle hypotonia. Both rapid-eye-movement (REM) sleep and increases in nasal pressure (PN) produce hypotonia, which persists even after nasal pressure is abruptly reduced. To determine the factors that influence the collapsibility of the hypotonic airway, the critical pressure (Pcrit) and nasal resistance upstream to the site of pharyngeal collapse (RN) were measured in the first three breaths after abrupt reductions in PN during non-REM and REM sleep. PN was reduced abruptly from 15.2+/-3.2 cm H2O (mean +/- SD) for three breaths in 19 apneic patients. Upper-airway pressure-flow relationships were analyzed to determine Pcrit for each breath in non-REM and REM sleep. We found that Pcrit rose (collapsibility increased, p < 0.001) and RN fell (p = 0.02) between the first and third breath after the decrease in PN, whereas no difference in Pcrit was detected between sleep stages. In six patients, genioglossus-muscle electromyograms (EMGs) were recorded. Peak phasic activity rose between the first and third breath (p = 0.03), but tonic and peak phasic EMG activity fell in REM as compared with non-REM sleep (p < 0.001). We conclude that the hypotonic upper airway becomes most collapsible by the third breath after an abrupt decrease in PN, regardless of sleep stage and despite an increase in genioglossus-muscle activity. Our findings suggest that predominantly mechanical rather than neuromuscular factors modulate the properties of the pharynx after abrupt reductions in nasal pressure.

PMID:
9563718
DOI:
10.1164/ajrccm.157.4.9706067
[Indexed for MEDLINE]
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