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PubMed2003

Genetics of sleep and sleep disorders.

Sleep has been observed in all vertebrates studied and in several invertebrates, notably the fruit fly Drosophila melanogaster. In all species, a substantial portion of life is spent in this behavioral state and disturbed sleep or lack of sleep has immediate negative impacts on performance and health. Although it is agreed upon that sleep fulfills a fundamental biological need, the function of sleep remains an enigma. Because the expression and regulation of sleep and some sleep disorders have strong genetic components, the recent progress in human, mouse, and fruit-fly genome sequencing projects have given rise to the expectation that the molecular pathways underlying sleep disorders and sleep regulation or even function can now be more readily identified. We review here available genetic data both from basic sleep research and sleep disorders with emphasis on recent advances in our understanding of the molecular basis of the homeostatic regulation of sleep. Recent studies in the dog, the mouse, and the fruit-fly have begun to reveal exciting new molecular pathways that regulate sleep. This illustrates that only the continued use of multiple animal models and genetic approaches will ensure a rapid progress in the relatively new field of sleep genetics.

Animals↗
PubMed2002

[Sleep hypoxemia during CPAP treatment in patients with obstructive sleep apnoea syndrome with chronic hypercapnia].

UNLABELLED: The aim of the study was to find the clinical features of the hypercapnic OSA patients, indicating possible failure of CPAP treatment in preventing sleep hypoxemia. The material of the study consisted of 37 hypercapnic OSA patients (age 49 +/- 9 years, apnea index 50 +/- 15, daytime PaCO2 52 +/- 6 mm Hg). In 1 patient arterial oxygen desaturation persisted because of the replacement of all mixed apnoeas by central apnoeas. In 26 patients SaO2 during CPAP treatment (85 +/- 27% in NREM and 72 +/- 12% in REM sleep) was lower during sleep than baseline SaO2 (91 +/- 2%, p < 0.05), in spite of disappearance of sleep apnoeas. In this group of patients there was more profound desaturation during sleep apnoeas (mean low SaO2 in NREM sleep 69 +/- 11% vs 84 +/- 4% and in REM sleep 50 +/- 8% vs 71 +/- 3% p < 0.001) and longer maximal apnea duration in NREM sleep (85 +/- 36s vs 56 +/- 23s, p < 0.01); in 24 of these patients there were the episodes of desaturation (mean SaO2 72 +/- 13%) during sleep lasting 2-6 min (mean 4 +/- 2 min) and in 16 patients (67%) there was secondary erythrocytosis. CONCLUSION: Hypoxemia during sleep in spite of disappearance of sleep apneas may occur in some hypercapnic, extremely obese OSA patients with ventilatory insufficiency, secondary erythrocytosis, profound arterial oxygen desaturation during sleep apnoeas and extremely long apnoeas during NREM sleep and with the signs of coexisting sleep hypoventilation syndrome.

Adult↗
PubMed1990

Sleep and sleep deprived EEG in partial and generalized epilepsy.

Sleep and sleep deprivation are often used for EEG activation in epilepsy. We compared postprandial naps and day-long sleep deprived EEGs in 36 patients with generalized seizures, 57 complex partial seizure patients, and 7 individuals with mixed seizure disorders. Ten of 36 generalized seizure patients had normal sleep and sleep deprived EEGs, while both were normal in 16 of 57 partial seizure patients. Both were abnormal in 18 of 36 generalized and 22 of 57 partial epileptics. Seven generalized seizure patients had epileptiform discharges or seizures during afternoon naps but normal sleep deprived EEGs. No partial seizure patients had normal sleep deprived EEGs and abnormal nap, but 29 of 57 had abnormalities or seizures only with sleep deprivation. All 7 mixed seizure patients had abnormal sleep and sleep deprived studies, and 6 had seizures, 4 on both studies. Natural sleep may facilitate the appearance of generalized seizures or epilepti-form discharges, while sleep deprivation may accentuate the yield of EEG abnormality in partial epilepsy. Either is likely to be abnormal in patients with mixed seizures and encephalopathy. Natural sleep and sleep deprived EEGs are an appropriate combination in the evaluation of refractory seizures.

Adolescent↗
PubMed1989

Electroencephalographic sleep in panic disorder. A focus on sleep-related panic attacks.

Sleep electroencephalograms were studied in 13 patients with panic disorder, six of whom experienced panic from sleep, and seven controls. Sleep was disturbed in the patients, as manifested by increased sleep latency, decreased sleep time, and decreased sleep efficiency. Rapid eye movement (REM) latencies were not reduced in the patient group. All six of the panic awakenings were preceded by non-REM sleep, which could be further characterized as a transition from stage II toward delta sleep. The overall degree of sleep disturbance (ie, sleep latency, sleep efficiency) did not appear to be influenced by the occurrence of sleep panic. There was also an association of increased REM latency with nights of sleep panic.

Adult↗
PubMed1986

Ultrashort sleep-waking schedule. III. 'Gates' and 'forbidden zones' for sleep.

Three experiments which utilized an ultrashort sleep-waking cycle were conducted to investigate the 24 h structure of sleepiness after 1 night of sleep deprivation under 2 experimental conditions: instructing subjects to attempt to fall asleep or instructing subjects to attempt to resist sleep. Six subjects participated in experiment 1. At 19.00 h they started a 13 min waking-7 min sleep attempt, or 13 min waking-7 min resisting sleep, until 19.00 h on the next day. Eight subjects were tested in a similar way in experiment 2, which started at 07.00 h after a night of sleep deprivation and lasted for 24 h. Eight subjects were similarly tested in experiment 3 which started at 11.00 h after a night of sleep deprivation and lasted for 36 h until 23.00 h on the next day. The results showed that in spite of the significant between-group differences in total sleep, the temporal structure of sleepiness was very similar in the 3 experiments. In each there was a bimodal distribution of sleepiness: a major nocturnal sleepiness crest and a secondary mid-afternoon sleepiness peak. These were separated by a 'forbidden zone' for sleep centred at around 20.00-22.00 h. The onset of the nocturnal sleep period (the sleep gate) was found to be a discrete event occurring as an 'all or none' phenomenon. Its timing was stable over a 2 week period, and independent of the specific experimental demands; there were no significant differences between the AS and RS conditions with respect to total sleep time or any of the sleep stages. These results, which demonstrate structured variations in sleepiness across the nycthemeron are discussed in the light of the recent modelling of sleep along homeostatic principles.

Adult↗
PubMed1989

Infrequent periodic sleep disruption: effects on sleep, performance and mood.

In the first of two experiments, 12 normal young adults had their sleep periodically disturbed for two nights in the laboratory at three different rates: 10 min of sleep followed by 20 min of disturbance, 20 min of sleep followed by 40 min of disturbance and 40 min of sleep followed by 80 min of disturbance. Sleep and disturbance alternated throughout the night. While all disturbance conditions resulted in decreased daytime performance and increased sleepiness, the disturbance conditions did not differ from each other. In the second experiment, sleep was periodically disturbed for two nights at three new rates to act as control conditions for Experiment 1. The three conditions were: 2 min of sleep followed by 4 min of disturbance, 20 min of sleep followed by a single awakening, and 40 min of sleep followed by a single awakening. Sleep and disturbance again alternated throughout the night. As expected, sleep was less disturbed and daytime decrements were smaller in the conditions allowing 20 and 40 min of sleep followed by a single awakening. The data from both experiments were interpreted as support for sleep continuity theory; i.e., as the length of periods of consolidated sleep decrease, residual decrements increase.

Adolescent↗
PubMed1999

Olanzapine acute administration in schizophrenic patients increases delta sleep and sleep efficiency.

BACKGROUND: A delta sleep deficit has been observed in schizophrenic patients. Olanzapine is a novel atypical antipsychotic agent with affinity at dopaminergic, serotonergic, muscarinic, adrenergic and histaminergic binding sites. The present study was designed to analyze a sleep promoting effect reported for olanzapine. METHODS: Twenty schizophrenic patients (DSM-IV) were studied, who were drug free and inpatients. Patients slept for 5 consecutive nights in the sleep unit as follows: one acclimatization night; two baseline nights (the first for sleep disorder screenings); and two olanzapine nights (10 mg olanzapine, one hour before sleep onset). RESULTS: Sleep continuity variables and total sleep time showed an overall improvement with olanzapine. Waking time was reduced since the first night of olanzapine administration. The main sleep architecture changes were: reduction in sleep stage 1, while sleep stage 2 and delta were significantly enhanced. Rapid eye movement density was also increased by the second olanzapine night. CONCLUSIONS: Total sleep improvement was due to the increase in sleep stages 2 and delta sleep. This may be related to serotonergic antagonistic properties of olanzapine. Olanzapine seems to have a sleep promoting effect in schizophrenic patients.

Adult↗
PubMed1999

A preliminary study of the effects of correction of anemia with recombinant human erythropoietin therapy on sleep, sleep disorders, and daytime sleepiness in hemodialysis patients (The SLEEPO study).

End-stage renal disease (ESRD) is commonly associated with complaints of disturbed sleep and sleep disorders, frequently related to periodic limb movements in sleep (PLMS) or sleep apnea that may result in daytime sleepiness and other sequelae. Improvements in quality of life, including subjective sleep quality, have been reported in ESRD patients treated with recombinant human erythropoietin (rHuEPO). We investigated the objective effects of normalizing hematocrit on sleep disorders, sleep patterns, and daytime ability to remain awake in ESRD patients. Ten hemodialysis patients with sleep complaints while on rHuEPO therapy were studied by polysomnography while moderately anemic (mean hematocrit, 32.3%) and again when hematocrit was normalized (mean hematocrit, 42.3%) by increased rHuEPO dosing. Sleep patterns and associated parameters were monitored. Delivered dialysis dose and iron storage factors were monitored. Maintenance of Wakefulness Testing (MWT) was performed to assess daytime alertness/sleepiness. All 10 subjects experienced highly statistically significant reductions in the total number of arousing PLMS (P = 0.002). Nine of 10 subjects showed reductions in both the Arousing PLMS Index (P < 0.01) and the PLMS Index (P = 0.03) when hematocrit was normalized. Measures of sleep quality showed trends to improved quality of sleep. MWT demonstrated significant improvement in the length of time patients were able to remain awake (9.7 versus 17.1 minutes; P = 0.04). RHuEPO therapy with full correction of anemia reduces PLMS, arousals from sleep, and sleep fragmentation while allowing for more restorative sleep and improved daytime alertness. These findings may explain one mechanism for the improved quality-of-life parameters reported in ESRD patients treated with rHuEPO.

Adult↗
PubMed2002

Sleep logs of young adults with self-selected sleep times predict the dim light melatonin onset.

The purpose of this study was to determine whether a sleep log parameter could be used to estimate the circadian phase of normal, healthy, young adults who sleep at their normal times, and thus naturally have day-to-day variability in their times of sleep. Thus, we did not impose any restrictions on the sleep schedules of our subjects (n = 26). For 14 d, they completed daily sleep logs that were verified with wrist activity monitors. On day 14, salivary melatonin was sampled every 30 min in dim light from 19:00 to 07:30 h to determine the dim light melatonin onset (DLMO). Daily sleep parameters (onset, midpoint, and wake) were taken from sleep logs and averaged over the last 5, 7, and 14 d before determination of the DLMO. The mean DLMO was 22:48 +/- 01:30 h. Sleep onset and wake time averaged over the last 5 d were 01:44 +/- 01:41 and 08:44 +/- 01:26 h, respectively. The DLMO was significantly correlated with sleep onset, midpoint, and wake time, but was most strongly correlated with the mean midpoint of sleep from the last 5 d (r = 0.89). The DLMO predicted using the mean midpoint of sleep from the last 5 d was within 1 h of the DLMO determined from salivary melatonin for 92% of the subjects; in no case did the difference exceed 1.5 h. The correlation between the DLMO and the score on the morningness-eveningness questionnaire was significant but comparatively weak (r = -0.48). We conclude that the circadian phase of normal, healthy day-active young adults can be accurately predicted using sleep times recorded on sleep logs (and verified by actigraphy), even when the sleep schedules are irregular.

Adolescent↗
PubMed1988

Passive body heating and sleep: influence of proximity to sleep.

Previous studies have found enhanced delta sleep following body heating. This study assessed the influence of body heating as a function of its proximity to sleep. Electroencephalogram (EEG) sleep patterns were compared following body heating (1 h immersion in water at 41 degrees C) at each of four times of day: morning (MO), afternoon (AF), early evening (EE), and late evening (LE), ending just prior to sleep. A delta filter/integrator system provided objective measures of delta content. Relative to baseline nights, whole-night delta sleep was increased by the two evening heating sessions only, particularly LE heating. Following LE, the increased delta occurred primarily in the first sleep cycle, whereas EE heating elicited increased delta distributed across the later sleep cycles (cycles 2-4). Effects on manually staged indices of slow wave sleep (SWS) were confined to increases in Stage 4 in the first sleep cycle following LE heating. Heating just prior to sleep also resulted in a substantial reduction in the duration of the first rapid eye movement sleep period. Sleep onset time was reduced by heating, particularly EE heating. The results indicate that body heating induces temporary changes that affect sleep propensity and both the quantity and temporal distribution of delta activity in the sleep EEG.

Adult↗
PubMed1994

Regulation of sleep rate and circadian consolidation of sleep and wakefulness in an infant.

Observations of sleep and wakefulness were continuously made over an infant's first 6 months by Kleitman and Engelmann. Those data have been reanalyzed using a newly developed tool, fractional-time analysis, and two measures derived from it: 1) sleep rate, the rate at which the infant accumulated sleep; and 2) consolidation, the degree to which episodes of sleep and wakefulness were sustained and clustered. Changes in sleep rate and consolidation were independent and were attributed to separate underlying neural mechanisms. Consolidation increased over the 6-month course of development. This was explained by the development of circadian rhythmicity, which appeared during the 1st month as a free-running, endogenously generated rhythm in sleep-episode durations. Starting in the 2nd month, sleep rate was regulated, and it remained remarkably stable for weeks at a time. Sleep rate decreased over the 6-month period, perhaps because metabolic rate decreased as the infant grew. Short-term (weeks-long) changes in consolidation and sleep rate were explained by "beating" of the non-24-hour, endogenous sleep rhythm with direct effects of the 24-hour environment on sleep and wakefulness. Environmental stimuli eventually entrained the circadian pacemaker, bringing the consolidating periods of wakefulness and sleep into register with day and night. The infant was thereby efficiently exposed to periodic sensory and social stimuli, promoting normal neural development. A model of sleep-wake regulation based on independent mechanisms for circadian timing and sleep-wake regulation is proposed.

Circadian Rhythm↗
PubMed1998

Homeostatic regulation of REM sleep in humans during extended sleep.

Benington and Heller (1994) recently proposed a sleep-dependent model for the homeostatic control of REM sleep in which the amount of REM sleep propensity discharged in each bout of REM sleep affects the timing of the subsequent REM episode. Consistent with their hypothesis, they reported that in rats the duration of a REM episode was positively correlated with the duration of the succeeding NREM episode and not with the duration of the preceding NREM episode. To assess this hypothesis in humans, we used 308 sleep records from 11 subjects who remained at bedrest in the dark and slept ad libitum during 14-hour periods each night for 4 weeks. The timing of the onset of the first REM episode of the long night was linked to the timing of sleep onset. NREM-REM cycle duration decreased progressively throughout the night as a result of a progressive decrease in duration of the NREM component. Durations of REM sleep episodes correlated significantly with durations of subsequent NREM episodes in three out of the eight rank cycles analyzed (p < .0031, Bonferroni corrected); positive correlation coefficients were found for all the remaining cycles, but were not statistically significant when the conservative Bonferroni correction of the alpha level was applied. With the exception of the first sleep cycle, durations of REM sleep episodes did not correlate with durations of preceding NREM sleep episodes. According to the present results, the amount of REM sleep in one episode controls the time of occurrence of the next REM episode when the impact of other possible regulating factors are at a low level. We hypothesize that the extended dark/rest period, by increasing the time window allowed for sleep, provided a condition under which the systems governing REM sleep expression were free of the masking imposed by the conventional 16 hours light/8 hours dark schedule that consolidates and compresses sleep.

Adult↗
PubMed2005

Sleep in adults with attention-deficit/hyperactivity disorder: a controlled polysomnographic study including spectral analysis of the sleep EEG.

STUDY OBJECTIVES: Previous studies in children with attention-deficit/hyperactivity disorder and attention deficit disorder (ADHD/ADD) have shown impaired sleep quality with increased nocturnal motor activity. However, polysomnographic findings are not unequivocal. Up to now, in adults with ADHD, only 1 case-control polysomnographic study with small sample size has been performed. We investigated objective and subjective sleep quality in adultADHD, including an electroencephalogram spectral power analysis. DESIGN: Single-blind comparative study. SETTING: University medical center. PARTICIPANTS: Twenty adult unmedicated ADHD patients without current comorbid major depression, drug abuse, or comorbid axis-II disorder and 20 sex- and age-matched control subjects. INTERVENTIONS: N/A. MEASUREMENTS: Conventional polysomnographic parameters and sleep electroencephalogram spectral power analysis was calculated for the 2 laboratory nights. Subjective sleep parameters were estimated by sleep questionnaires to assess the relationship between objective and subjective sleep measurements. RESULTS: Adult ADHD patients showed increased nocturnal motor activity (as indicated by heightened indexes of periodic leg movements in sleep), which was significantly inversely correlated with subjective total sleep time. Although ADHD patients displayed significantly increased objective total sleep time, the subjective ratings documented impaired sleep quality in those with ADHD. Other polysomnographic sleep patterns and spectral electroencephalogram parameters did not differ between ADHD patients and normal controls. CONCLUSIONS: Similar to children, adults with ADHD show increased nocturnal motor activity. Otherwise, sleep does not seem to be impaired in ADHD patients. However, the dissociation between objective and subjective sleep parameters points to a misinterpretation of sleep quality in patients with ADHD.

Adult↗
PubMed2006

The effect of donepezil on sleep and REM sleep EEG in patients with Alzheimer disease: a double-blind placebo-controlled study.

STUDY OBJECTIVE: Examine the effects of donepezil on sleep and rapid eye movement (REM) sleep electroencephalogram (EEG) in patients with Alzheimer disease, using polysomnography, and the correlation between REM sleep EEG parameters and cognitive scores. DESIGN: Randomized, double-blind, placebo-controlled design. SETTINGS: Two sleep research centers, University Hospital. PARTICIPANTS: Thirty-five patients with mild to moderate Alzheimer disease, allocated to 2 groups: donepezil treated (n=17) and placebo treated (n=18). INTERVENTION: Patients were administered donepezil or placebo. OUTCOME MEASURES: Polysomnography with REM sleep EEG spectral analysis and cognitive evaluation using the Alzheimer Disease Assessment Scale, cognitive subscale, were performed at baseline and after 3 and 6 months. Slowing ratio was the ratio between slow and fast EEG frequency bands. Cognitive and sleep data were analyzed using analysis of variance. Correlations between cognitive improvement and REM sleep EEG were also calculated. RESULTS: REM sleep increased significantly after 3 and 6 months of donepezil treatment compared with baseline and placebo (p < .01). Overall theta (p = .04), frontal theta (p < .01) and frontal delta (p = .03) absolute power during REM sleep decreased after 6 months of donepezil treatment. The occipital slowing ratio decreased during treatment (p = .04). REM sleep overall and frontal and centroparietal alpha absolute power significantly correlated with the cognitive improvement rate on the Alzheimer Disease Assessment Scale, cognitive subscale (r = 0.75, r = 0.71, r = 0.78); p < .01). CONCLUSIONS: Donepezil treatment enhanced REM sleep and reduced slow frequencies of REM sleep EEG, suggesting a possible action upon REM sleep-related cholinergic neurons in patients with Alzheimer disease. Furthermore, REM sleep alpha power may predict the cognitive response to donepezil.

Aged↗
PubMed1982

Dynamic relation of sleep spindles and K-complexes to spontaneous phasic arousal in sleeping human subjects.

K-complexes unaccompanied by sleep spindles (K0-complexes) and isolated sleep spindles during stage 2, non-rapid eye movement (NREM) sleep were examined before and after transient activation phase (AP) and also pseudo-AP during human sleep to determine the relationship of K0-complexes and sleep spindles to APs. Sixteen sleep records obtained from 16 young adult males were scanned for isolated APs during stage 2 NREM sleep. One hundred APs and 62 pseudo-APs were identified and analyzed. The number of sleep spindles decreased and reached its minimum at the onset of APs, when an increase was observed in the number of K0-complexes. APs occurred when a decrease in sleep spindles was coupled with an increased incidence of K0-complexes, thus forming an antagonistic relation. A similar antagonism was observed between sleep spindles and slow waves. A working hypothesis was formulated to interpret a triad of sleep events: sleep spindles. K0-complexes, and slow wave sleep. Three kinds of sleep--REM, spindles-dominant, and slow-wave-dominant--are suggested as more useful classifications than the Rechtschaffen and Kales categories.

Adult↗
PubMed1997

Autonomic cardiac regulation in obstructive sleep apnea syndrome: evidence from spontaneous baroreflex analysis during sleep.

OBJECTIVE: To assess spontaneous baroreceptor-heart rate reflex sensitivity during sleep in patients with obstructive sleep apnea syndrome, a condition associated with increased cardiovascular morbidity and mortality and characterized by marked sympathetic activation, which is believed to originate from hypoxic chemoreceptor stimulation, although little is known of other possible mechanisms such as baroreflex impairment. DESIGN AND METHODS: In 11 patients with severe obstructive sleep apnea syndrome (mean+/-SD age 46.8+/-8.1 years, apnea/hypopnea index 67.9+/-19.1 h), who were normotensive or borderline hypertensive during wakefulness by clinic blood pressure measurements, finger blood pressure was monitored beat-by-beat non-invasively (Finapres) at night during polysomnography. Periods of wakefulness and sleep were identified based on electroencephalographic recordings. Baroreflex sensitivity was assessed by the sequence technique, as the slope of the regression line between spontaneous increases or reductions in systolic blood pressure (SBP) and the related lengthening or shortening in the RR interval, occurring over spontaneous sequences of four or more consecutive beats. The number of these sequences was also computed, as an additional index of baroreflex engagement by the spontaneous blood pressure fluctuations. The controls were age-related normotensive or borderline hypertensive subjects without sleep apnea who had been investigated in previous studies; in these subjects blood pressure was recorded intra-arterially over 24 h in ambulatory conditions and spontaneous baroreflex sensitivity was assessed by the sequence technique. RESULTS: In our patients the lowest nocturnal arterial oxygen saturation was 78.6+/-12.1% (mean+/-SD). During sleep, the number of pooled +RR/+SBP and -RR/-SBP sequences per hour was 20.3+/-2.7 per h in patients with sleep apnea and 27.1+/-2.1 /h in controls (means+/-SEM). The average baroreflex sensitivity during sleep periods was 7.04+/-0.8 ms/mmHg in sleep apnea patients and 10.05+/-2.1 ms/mmHg in controls. Both the pooled number of sequences and baroreflex sensitivity values of the sleep apnea patients were significantly (P < 0.01) less than the corresponding night values of control subjects. In the sleep apnea patients, at variance from controls, baroreflex sensitivity did not show any increase during sleep compared with its values during wakefulness (6.9+/-1.0 ms/mmHg). CONCLUSIONS: Our data provide evidence that spontaneous baroceptor reflex sensitivity is depressed in severe obstructive sleep apnea syndrome. This suggests that in such patients baroreflex dysfunction and not only chemoreceptor stimulation by hypoxia may be involved in the sympathetic activation which occurs during sleep. Such dysfunction may contribute to the higher rate of cardiovascular morbidity and mortality reported in these patients.

Adult↗
PubMed2002

Selective REM sleep deprivation during daytime I. Time course of interventions and recovery sleep.

Although repeated selective rapid eye movement (REM) sleep deprivation by awakenings during nighttime has shown that the number of sleep interruptions required to prevent REM sleep increases within and across consecutive nights, the underlying regulatory processes remained unspecified. To assess the role of circadian and homeostatic factors in REM sleep regulation, REM sleep was selectively deprived in healthy young adult males during a daytime sleep episode (7-15 h) after a night without sleep. Circadian REM sleep propensity is known to be high in the early morning. The number of interventions required to prevent REM sleep increased from the first to the third 2-h interval by a factor of two and then leveled off. Only a minor REM sleep rebound (11.6%) occurred in the following undisturbed recovery night. It is concluded that the limited rise of interventions during selective daytime REM sleep deprivation may be due to the declining circadian REM sleep propensity, which may partly offset the homeostatic drive and the sleep-dependent disinhibition of REM sleep.

Adult↗
PubMed1980

Effect of sleep fragmentation on ventilatory and arousal responses of sleeping dogs to respiratory stimuli.

We studied the effects of sleep fragmentation on arousal and ventilatory responses to hyperoxic hypercapnia, isocapnic hypoxia, and chemical stimulation of the larynx during sleep in 5 dogs. Sleep fragmentation was induced by repeatedly arousing the dogs with acoustic stimuli throughout 2 to 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 electroencephalographic and behavioral criteria. Hypercapnic and hypoxic ventilatory responses were unimpaired by sleep fragmentation. In contrast, alveolar PCO2 levels at arousal increased after sleep fragmentation, from a mean +/- SEM 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 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 rapid-eye-movement sleep. Arousal responses to laryngeal stimulation were also impaired after sleep fragmentation. We conclude that arousal responses to respiratory stimuli are decreased by sleep fragmentation.

Animals↗