TY - JOUR
T1 - Effect of sleep deprivation on responses to airway obstruction in the sleeping dog
AU - O'Donnell, C. P.
AU - King, E. D.
AU - Schwartz, A. R.
AU - Smith, P. L.
AU - Robotham, J. L.
PY - 1994/1/1
Y1 - 1994/1/1
N2 - The effect of sleep deprivation on sleep architecture and respiratory responses to repetitive airway obstruction during sleep was investigated in four chronically instrumented tracheostomized dogs during 12-h nocturnal experiments. A 24-h period of prior sleep deprivation increased (P < 0.05) the rate at which airway obstruction could be induced from 20 ± 3 (SE) to 37 ± 10 times/h compared with non-sleep-deprived dogs. During non-rapid-eye- movement sleep the duration of obstruction, minimum arterial hemoglobin saturation, and peak negative inspiratory effort at arousal were 20.5 ± 1.0 s, 91.7 ± 0.5%, and 28.4 ± 1.8 mmHg, respectively, in non-sleep-deprived dogs. Sleep deprivation increased (P < 0.01) the duration of obstruction to 28.0 ± 0.9 s, worsened (P < 0.05) the minimal arterial hemoglobin desaturation to 85.4 ± 3.1%, and increased (P < 0.025) the peak negative inspiratory effort at arousal to 36.1 ± 1.6 mmHg. Sleep deprivation also caused increases (P < 0.025) in total sleep time, rapid-eye-movement (REM) sleep time, and percentage of time in REM sleep in a 2-h recovery period without airway obstruction at the end of the study. We conclude that airway obstruction in the sleeping dog can reproduce the disturbances in sleep architecture and respiration that occur in obstructive sleep apnea and that prior sleep deprivation will increase apnea severity, degree of somnolence, and REM sleep rebound independent of change in upper airway collapsibility.
AB - The effect of sleep deprivation on sleep architecture and respiratory responses to repetitive airway obstruction during sleep was investigated in four chronically instrumented tracheostomized dogs during 12-h nocturnal experiments. A 24-h period of prior sleep deprivation increased (P < 0.05) the rate at which airway obstruction could be induced from 20 ± 3 (SE) to 37 ± 10 times/h compared with non-sleep-deprived dogs. During non-rapid-eye- movement sleep the duration of obstruction, minimum arterial hemoglobin saturation, and peak negative inspiratory effort at arousal were 20.5 ± 1.0 s, 91.7 ± 0.5%, and 28.4 ± 1.8 mmHg, respectively, in non-sleep-deprived dogs. Sleep deprivation increased (P < 0.01) the duration of obstruction to 28.0 ± 0.9 s, worsened (P < 0.05) the minimal arterial hemoglobin desaturation to 85.4 ± 3.1%, and increased (P < 0.025) the peak negative inspiratory effort at arousal to 36.1 ± 1.6 mmHg. Sleep deprivation also caused increases (P < 0.025) in total sleep time, rapid-eye-movement (REM) sleep time, and percentage of time in REM sleep in a 2-h recovery period without airway obstruction at the end of the study. We conclude that airway obstruction in the sleeping dog can reproduce the disturbances in sleep architecture and respiration that occur in obstructive sleep apnea and that prior sleep deprivation will increase apnea severity, degree of somnolence, and REM sleep rebound independent of change in upper airway collapsibility.
KW - arousal
KW - endotracheal tube
KW - hemoglobin saturation
KW - hypoxia
KW - non-rapid-eye-movement sleep
KW - rapid-eye-movement sleep
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U2 - 10.1152/jappl.1994.77.4.1811
DO - 10.1152/jappl.1994.77.4.1811
M3 - Article
C2 - 7836204
AN - SCOPUS:0028149295
SN - 8750-7587
VL - 77
SP - 1811
EP - 1818
JO - Journal of applied physiology
JF - Journal of applied physiology
IS - 4
ER -