Effect of sleep deprivation on responses to airway obstruction in the sleeping dog

1994 ◽  
Vol 77 (4) ◽  
pp. 1811-1818 ◽  
Author(s):  
C. P. O'Donnell ◽  
E. D. King ◽  
A. R. Schwartz ◽  
P. L. Smith ◽  
J. L. Robotham

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.

Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Xiaoyue Liu ◽  
Jeongok G Logan ◽  
Younghoon Kwon ◽  
Jennifer Lobo ◽  
Hyojung Kang ◽  
...  

Introduction: Blood pressure (BP) variability (BPV) is a novel marker for cardiovascular disease (CVD) independent of high BP. Sleep architecture represents the structured pattern of sleep stages consisting of rapid eye movement (REM) and non-rapid eye movement (NREM), and it is an important element in the homeostatic regulation of sleep. Currently, little is known regarding whether BPV is linked to sleep stages. Our study aimed to examine the relationship between sleep architecture and BPV. Methods: We analyzed in-lab polysomnographic studies collected from individuals who underwent diagnostic sleep studies at a university hospital from 2010 to 2017. BP measures obtained during one year prior to the sleep studies were included. BPV was computed using the coefficient of variation for all individuals who had three or more systolic and diastolic BP data. We conducted linear regression analysis to assess the relationship of systolic BPV (SBPV) and diastolic BPV (DBPV) with the sleep stage distribution (REM and NREM sleep time), respectively. Covariates that can potentially confound the relationships were adjusted in the models, including age, sex, race/ethnicity, body mass index, total sleep time, apnea-hypopnea index, mean BP, and history of medication use (antipsychotics, antidepressants, and antihypertensives) during the past two years before the sleep studies. Results: Our sample (N=3,565; male = 1,353) was racially and ethnically diverse, with a mean age 54 ± 15 years and a mean BP of 131/76 ± 13.9/8.4 mmHg. Among the sleep architecture measures examined, SBPV showed an inverse relationship with REM sleep time after controlling for all covariates ( p = .033). We subsequently categorized SBPV into four quartiles and found that the 3 rd quartile (mean SBP SD = 14.9 ± 2.1 mmHg) had 3.3 fewer minutes in REM sleep compared to the 1 st quartile ( p = .02). However, we did not observe any relationship between DBPV and sleep architecture. Conclusion: Greater SBPV was associated with lower REM sleep time. This finding suggests a possible interplay between BPV and sleep architecture. Future investigation is warranted to clarify the directionality, mechanism, and therapeutic implications.


SLEEP ◽  
2019 ◽  
Vol 43 (6) ◽  
Author(s):  
Sjoerd J van Hasselt ◽  
Maria Rusche ◽  
Alexei L Vyssotski ◽  
Simon Verhulst ◽  
Niels C Rattenborg ◽  
...  

Abstract Most of our knowledge about the regulation and function of sleep is based on studies in a restricted number of mammalian species, particularly nocturnal rodents. Hence, there is still much to learn from comparative studies in other species. Birds are interesting because they appear to share key aspects of sleep with mammals, including the presence of two different forms of sleep, i.e. non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. We examined sleep architecture and sleep homeostasis in the European starling, using miniature dataloggers for electroencephalogram (EEG) recordings. Under controlled laboratory conditions with a 12:12 h light–dark cycle, the birds displayed a pronounced daily rhythm in sleep and wakefulness with most sleep occurring during the dark phase. Sleep mainly consisted of NREM sleep. In fact, the amount of REM sleep added up to only 1~2% of total sleep time. Animals were subjected to 4 or 8 h sleep deprivation to assess sleep homeostatic responses. Sleep deprivation induced changes in subsequent NREM sleep EEG spectral qualities for several hours, with increased spectral power from 1.17 Hz up to at least 25 Hz. In contrast, power below 1.17 Hz was decreased after sleep deprivation. Sleep deprivation also resulted in a small compensatory increase in NREM sleep time the next day. Changes in EEG spectral power and sleep time were largely similar after 4 and 8 h sleep deprivation. REM sleep was not noticeably compensated after sleep deprivation. In conclusion, starlings display signs of NREM sleep homeostasis but the results do not support the notion of important REM sleep functions.


2001 ◽  
Vol 90 (6) ◽  
pp. 2490-2501 ◽  
Author(s):  
Hedieh Hamrahi ◽  
Richard Stephenson ◽  
Safraaz Mahamed ◽  
Kiong Sen Liao ◽  
Richard L. Horner

Recurrent sleep-related hypoxia occurs in common disorders such as obstructive sleep apnea (OSA). The marked changes in sleep after treatment suggest that stimuli associated with OSA (e.g., intermittent hypoxia) may significantly modulate sleep regulation. However, no studies have investigated the independent effects of intermittent sleep-related hypoxia on sleep regulation and recovery sleep after removal of intermittent hypoxia. Ten rats were implanted with telemetry units to record the electroencephalogram (EEG), neck electromyogram, and body temperature. After >7 days recovery, a computer algorithm detected sleep-wake states and triggered hypoxic stimuli (10% O2) or room air stimuli only during sleep for a 3-h period. Sleep-wake states were also recorded for a 3-h recovery period after the stimuli. Each rat received an average of 69.0 ± 6.9 hypoxic stimuli during sleep. The non-rapid eye movement (non-REM) and rapid-eye-movement (REM) sleep episodes averaged 50.1 ± 3.2 and 58.9 ± 6.6 s, respectively, with the hypoxic stimuli, with 32.3 ± 3.2 and 58.6 ± 4.8 s of these periods being spent in hypoxia. Compared with results for room air controls, hypoxic stimuli led to increased wakefulness ( P < 0.005), nonsignificant changes in non-REM sleep, and reduced REM sleep ( P < 0.001). With hypoxic stimuli, wakefulness episodes were longer and more frequent, non-REM periods were shorter and more frequent, and REM episodes were shorter and less frequent ( P < 0.015). Hypoxic stimuli also increased faster frequencies in the EEG ( P < 0.005). These effects of hypoxic stimuli were reversed on return to room air. There was a rebound increase in REM sleep, increased slower non-REM EEG frequencies, and decreased wakefulness ( P < 0.001). The results show that sleep-specific hypoxia leads to significant modulation of sleep-wake regulation both during and after application of the intermittent hypoxic stimuli. This study is the first to determine the independent effects of sleep-related hypoxia on sleep regulation that approximates OSA before and after treatment.


1994 ◽  
Vol 77 (4) ◽  
pp. 1819-1828 ◽  
Author(s):  
C. P. O'Donnell ◽  
E. D. King ◽  
A. R. Schwartz ◽  
J. L. Robotham ◽  
P. L. Smith

The relationship between airway obstruction during sleep and changes in mean arterial pressure (MAP) was investigated in four chronically instrumented tracheostomized dogs during 12-h nocturnal experiments. The MAP response was determined 1) during experimental airway obstruction whenever sleep occurred, 2) over each 12-h experiment, and 3) during a 2-h recovery period at the end of each experiment. The effects of 24 h of sleep deprivation and changes in plasma levels of renin and atrial natriuretic peptide were assessed. In non-rapid-eye-movement sleep, a period of airway obstruction caused MAP to increase (P < 0.002) from 95 +/- 3 (SE) mmHg to 112 +/- 3 mmHg, and this difference was enhanced (P < 0.04) by sleep deprivation. There was an increase of 12 +/- 2 mmHg in the overall MAP over time (P < 0.001) in non-rapid-eye-movement sleep that was sustained in the 2-h recovery period. Plasma levels of renin and atrial natriuretic peptide were constant and unrelated to changes in MAP. We conclude that in the sleeping dog airway obstruction causes an increase in MAP that can be accentuated by prior sleep deprivation and that repetitive airway obstruction will cause an increase in MAP over time that is sustained for > or = 2 h when normal airway patency is restored.


1995 ◽  
Vol 268 (6) ◽  
pp. R1456-R1463 ◽  
Author(s):  
T. Porkka-Heiskanen ◽  
S. E. Smith ◽  
T. Taira ◽  
J. H. Urban ◽  
J. E. Levine ◽  
...  

Noradrenergic locus ceruleus neurons are most active during waking and least active during rapid eye movement (REM) sleep. We expected REM sleep deprivation (REMSD) to increase norepinephrine utilization and activate the tyrosine hydroxylase (TH) gene critical for norepinephrine production. Male Wistar rats were deprived of REM sleep with the platform method. Rats were decapitated after 8, 24, or 72 h on small (REMSD) or large (control) platforms or after 8 or 24 h of rebound sleep after 72 h of the platform treatment. During the first 24 h, norepinephrine concentration, measured by high-performance liquid chromatography/electrochemical detection, was lower in the neocortex, hippocampus, and posterior hypothalamus in REMSD rats than in large-platform controls. After 72 h of REMSD, TH mRNA, measured by in situ hybridization, was increased in the locus ceruleus and norepinephrine concentrations were increased. Polygraphy showed that small-platform treatment caused effective and selective REMSD. Serum corticosterone measurement by radioimmunoassay indicated that the differences found in norepinephrine and TH mRNA were not due to differences in stress between the treatments. The novel finding of sleep deprivation-specific increase in TH gene expression indicates an important mechanism of adjusting to sleep deprivation.


2018 ◽  
Vol 120 (1) ◽  
pp. 296-305 ◽  
Author(s):  
Mohsen Naji ◽  
Maxim Komarov ◽  
Giri P. Krishnan ◽  
Atul Malhotra ◽  
Frank L. Powell ◽  
...  

In patients with obstructive sleep apnea (OSA), the pharyngeal muscles become relaxed during sleep, which leads to a partial or complete closure of upper airway. Experimental studies suggest that withdrawal of noradrenergic and serotonergic drives importantly contributes to depression of hypoglossal motoneurons and, therefore, may contribute to OSA pathophysiology; however, specific cellular and synaptic mechanisms remain unknown. In this new study, we developed a biophysical network model to test the hypothesis that, to explain experimental observations, the neuronal network for monoaminergic control of excitability of hypoglossal motoneurons needs to include excitatory and inhibitory perihypoglossal interneurons that mediate noradrenergic and serotonergic drives to hypoglossal motoneurons. In the model, the state-dependent activation of the hypoglossal motoneurons was in qualitative agreement with in vivo data during simulated rapid eye movement (REM) and non-REM sleep. The model was applied to test the mechanisms of action of noradrenergic and serotonergic drugs during REM sleep as observed in vivo. We conclude that the proposed minimal neuronal circuit is sufficient to explain in vivo data and supports the hypothesis that perihypoglossal interneurons may mediate state-dependent monoaminergic drive to hypoglossal motoneurons. The population of the hypothesized perihypoglossal interneurons may serve as novel targets for pharmacological treatment of OSA. NEW & NOTEWORTHY In vivo studies suggest that during rapid eye movement sleep, withdrawal of noradrenergic and serotonergic drives critically contributes to depression of hypoglossal motoneurons (HMs), which innervate the tongue muscles. By means of a biophysical model, which is consistent with a broad range of empirical data, we demonstrate that the neuronal network controlling the excitability of HMs needs to include excitatory and inhibitory interneurons that mediate noradrenergic and serotonergic drives to HMs.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A214-A215
Author(s):  
C Zhang ◽  
H Xu ◽  
J Zou ◽  
J Guan ◽  
H Yi ◽  
...  

Abstract Introduction Obstructive sleep apnea (OSA) is increasingly associated with insulin resistance. The underlying pathophysiology remains unclear but rapid eye movement (REM) sleep has been hypothesized to play a key role. To investigate the associations of insulin resistance with respiratory events and sleep duration during REM sleep, 4,062 Han Chinese individuals with suspected OSA were screened and 2,899 were analyzed. Methods We screened 4,062 participants with suspected OSA who underwent polysomnography in our sleep center from 2009 to 2016. Polysomnographic variables, biochemical indicators, and physical measurements were collected. Logistic regression analyses were conducted to determine the odds ratios (ORs) and 95% confidence intervals (95% CIs) for insulin resistance as assessed by hyperinsulinemia, the homeostasis model assessment of insulin resistance (HOMA-IR), fasting insulin resistance index (FIRI), and Bennet’s insulin sensitivity index (ISI). Results The final analyses included 2,899 participants. After adjusting for age, gender, body mass index, waist circumference, mean arterial pressure, smoking status, alcohol consumption, and the apnea and hypopnea index during non-REM sleep (AHINREM), the results revealed that AHI during REM sleep (AHIREM) was independently associated with insulin resistance; across higher AHIREM quartiles, the ORs (95% CIs) for hyperinsulinemia were 1.340 (1.022, 1.757), 1.210 (0.882, 1.660), and 1.632 (1.103, 2.416); those for abnormal HOMA-IR were 1.287 (0.998, 1.661), 1.263 (0.933, 1.711), and 1.556 (1.056, 2.293); those for abnormal FIRI were 1.386 (1.048, 1.835), 1.317 (0.954, 1.818), and 1.888 (1.269, 2.807); and those for abnormal Bennet’s ISI were 1.297 (1.003, 1.678), 1.287 (0.949, 1.747), and 1.663 (1.127, 2.452) (P &lt; 0.01 for all linear trends). Additionally, the results showed that for every 1-h increase in REM duration, the risk of hyperinsulinemia decreased by 22.3% (P &lt; 0.05). Conclusion The present study demonstrated that AHIREM was independently associated with hyperinsulinemia and abnormal HOMA-IR, FIRI, and Bennet’s ISI. Additionally, REM sleep duration was independently associated with hyperinsulinemia. Support This study was supported by Grants-in-aid from Shanghai Municipal Commission of Science and Technology (No.18DZ2260200).


2022 ◽  
Vol 12 ◽  
Author(s):  
Xuan Zhang ◽  
Ning Zhang ◽  
Yang Yang ◽  
Shuo Wang ◽  
Ping Yu ◽  
...  

In order to explore the characteristics and treatment status of obstructive sleep apnea (OSA) patients with hypertension, a retrospective study was conducted on 306 patients admitted from October 2018 to December 2019. According to the apnea hypopnea index (AHI), OSA patients with hypertension were divided into three groups. 69 cases were mild OSA (5 ≤ AHI &lt; 15), 86 cases were moderate (15 ≤ AHI &lt; 30), and 151 cases were severe (AHI ≥ 30). Compared with patients in the mild and moderate groups, the severe group had more male patients, with higher body mass index (BMI) and non-rapid eye movement stage 1 accounted for total sleep time (N1%), and lower non-rapid eye movement stage 2 accounted for total sleep time (N2%), average and minimum blood oxygen. Among all the patients, those who underwent the titration test accounted for 20.6% (63/306). Multivariate analysis showed that sleep efficiency (p &lt; 0.001) and AHI (p &lt; 0.001) were independent factors for patients to accept titration test. OSA patients with hypertension had a low acceptance of titration therapy. These people with higher sleep efficiency and AHI were more likely to receive autotitration.


2016 ◽  
Vol 3 (10) ◽  
pp. 160201 ◽  
Author(s):  
Peter Achermann ◽  
Thomas Rusterholz ◽  
Roland Dürr ◽  
Thomas König ◽  
Leila Tarokh

Sleep is characterized by a loss of consciousness, which has been attributed to a breakdown of functional connectivity between brain regions. Global field synchronization (GFS) can estimate functional connectivity of brain processes. GFS is a frequency-dependent measure of global synchronicity of multi-channel EEG data. Our aim was to explore and extend the hypothesis of disconnection during sleep by comparing GFS spectra of different vigilance states. The analysis was performed on eight healthy adult male subjects. EEG was recorded during a baseline night, a recovery night after 40 h of sustained wakefulness and at 3 h intervals during the 40 h of wakefulness. Compared to non-rapid eye movement (NREM) sleep, REM sleep showed larger GFS values in all frequencies except in the spindle and theta bands, where NREM sleep showed a peak in GFS. Sleep deprivation did not affect GFS spectra in REM and NREM sleep. Waking GFS values were lower compared with REM and NREM sleep except for the alpha band. Waking alpha GFS decreased following sleep deprivation in the eyes closed condition only. Our surprising finding of higher synchrony during REM sleep challenges the view of REM sleep as a desynchronized brain state and may provide insight into the function of REM sleep.


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