EFFECT OF SLEEP FRAGMENTATION ON VENTILATORY AND AROUSAL RESPONSES OF SLEEPING DOGS TO RESPIRATORY STIMULI

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Abstract
The effects of sleep fragmentation on arousal and ventilatory responses to hyperoxic hypercapnia, isocapnic hypoxia, and chemical stimulation of the larynx were studied during sleep in 5 dogs. Sleep fragmentation was induced by repeatedly arousing the dogs with acoustic stimuli throughout 2-3 consecutive nights. Responses to respiratory stimuli were then studied during a subsequent daytime sleep. Arterial O2 saturation was measured with an ear oximeter, and sleep stage was determined by EEG and behavioral criteria. Hypercapnic and hypoxic ventilatory responses were unimpaired by sleep fragmentation. Alveolar PCO2 (partial pressure CO2) levels at arousal increased after sleep fragmentation, from a mean .+-. SEM (standard error of mean) of 52.2 .+-. 1.4 mm Hg to 55.6 .+-. 1.5 mm Hg (P < 0.05) during slow-wave sleep, and from 57.9 .+-. 1.5 mm Hg to 61.3 .+-. 2.2 mm Hg (P < 0.05) during rapid-eye-movement REM sleep. Similarly, arterial O2 saturation at arousal decreased after sleep fragmentation from 80.1 .+-. 1.0% to 70.2 .+-. 2.7% (P < 0.05) during slow-wave sleep, and from 66.3 .+-. 3.6% to < 55% (P < 0.05) during REM sleep. Arousal responses to laryngeal stimulation were also impaired after sleep fragmentation. Arousal responses to respiratory stimuli are decreased by sleep fragmentation. Implications for human sleep-apnea syndromes was discussed.