Cholinergic reticular mechanisms influence state-dependent ventilatory response to hypercapnia

1991 ◽  
Vol 261 (3) ◽  
pp. R738-R746 ◽  
Author(s):  
R. Lydic ◽  
H. A. Baghdoyan ◽  
R. Wertz ◽  
D. P. White
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Respiratory Control ◽  
Nrem Sleep ◽  
Neural Mechanisms ◽  
Rapid Eye Movement ◽  
State Dependent ◽  
First Time

Breathing is impaired by the loss of wakefulness that accompanies sleep, certain comatose states, and anesthesia. Although state-dependent decrements in breathing and the ability to respond to hypercapnic stimuli are characteristic of most mammals, the neural mechanisms that cause state-dependent changes in respiratory control remain poorly understood. The present study examined the hypothesis that cholinergic mechanisms in the medial pontine reticular formation (mPRF) can cause state-dependent changes in breathing and in the hypercapnic ventilatory response (HCVR). Six cats were anesthetized with halothane and chronically instrumented for subsequent studies of breathing during wakefulness, non-rapid-eye-movement (NREM) sleep, rapid-eye-movement (REM) sleep, and during the REM sleep-like state caused by mPRF microinjections of carbachol or bethanechol. Minute ventilation was significantly decreased during the carbachol-induced REM sleep-like state (DCarb) compared with wakefulness. The HCVR in NREM, REM, DCarb, and after bethanechol was less than the waking HCVR. These results show for the first time that cholinoceptive regions in the mPRF can cause state-dependent reductions in normocapnic minute ventilation and in the ventilatory response to hypercapnia.

Occlusion pressure and ventilation during sleep in normal humans

1986 ◽  
Vol 61 (4) ◽  
pp. 1279-1287 ◽  
Author(s):  
D. P. White
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Nrem Sleep ◽  
Respiratory Drive ◽  
Rapid Eye Movement ◽  
System Sensitivity ◽  
Hypercapnic Ventilatory Response ◽  
Normal Humans

Previous investigation in normal humans has demonstrated reduced ventilation and ventilatory responses to chemical stimuli during sleep. Most have interpreted this to be a product of decreasing central nervous system sensitivity to the normal stimuli that maintain ventilation, whereas other factors such as increasing airflow resistance could also contribute to this reduction in respiration. To improve our understanding of these events, we measured ventilation and occlusion pressures (P0.1) during unstimulated ventilation and rebreathing-induced hypercapnia during wakefulness and non-rapid-eye-movement (NREM) and rapid-eye-movement (REM) sleep. Eighteen subjects (10 males and 8 females) of whom seven were snorers (5 males and 2 females) were studied. Ventilation was reduced during both NREM and REM sleep (P less than 0.05), but this decrement in minute ventilation tended to be greater in snorers than nonsnorers. Unstimulated P0.1, on the other hand, was maintained or increased during sleep in all groups studied, with males and snorers showing the largest increase. The hypercapnic ventilatory response fell during both NREM and REM sleep and tended to be lower during REM than NREM sleep. However, the P0.1 response to hypercapnia during NREM sleep was well maintained at the waking level although the REM response was statistically reduced. These studies suggest that the mechanism of the reduction in ventilation and the hypercapnic ventilatory response seen during sleep, particularly NREM sleep, is likely to be multifactorial and not totally a product of decreasing central respiratory drive.

Congenital Central Hypoventilation and Sleep State

PEDIATRICS ◽  
1980 ◽  
Vol 66 (3) ◽  
pp. 425-428
Author(s):  
Peter J. Fleming ◽  
Darlene Cade ◽  
M. Heather Bryan ◽  
A. Charles Bryan
Keyword(s):  
Metabolic Control ◽  
Eye Movement ◽  
Rem Sleep ◽  
Ventilatory Response ◽  
Respiratory Control ◽  
Rapid Eye Movement ◽  
Sleep State ◽  
Quiet Sleep ◽  
Awake State ◽  
Central Hypoventilation

Congenital central hypoventilation (Ondine's curse) is described in an infant with persistant symptoms throughout the first nine months of life. Respiratory control was most severely affected in quiet sleep, although abnormalities were present in rapid eye movement (REM) sleep and while awake. Failure of metabolic control in quiet sleep led to profound hypoventilation. Behavioral or "behavioral-like" inputs in the awake state and REM sleep increased ventilation, but not to expected normal levels. The ventilatory response to inhaled 4% CO2 was markedly depressed in all states.

Ventilatory behavior during sleep among A/J and C57BL/6J mouse strains

2004 ◽  
Vol 97 (5) ◽  
pp. 1787-1795 ◽  
Author(s):  
Lee Friedman ◽  
Abby Haines ◽  
Ken Klann ◽  
Laura Gallaugher ◽  
Lawrence Salibra ◽  
...  
Keyword(s):  
Heart Rate ◽  
Eye Movement ◽  
Rem Sleep ◽  
Minute Ventilation ◽  
Inbred Mouse ◽  
Nrem Sleep ◽  
Mouse Strains ◽  
Rapid Eye Movement ◽  
Breathing Patterns ◽  
Strain Interaction

The pattern of breathing during sleep could be a heritable trait. Our intent was to test this genetic hypothesis in inbred mouse strains known to vary in breathing patterns during wakefulness (Han F, Subramanian S, Dick TE, Dreshaj IA, and Strohl KP. J Appl Physiol 91: 1962–1970, 2001; Han F, Subramanian S, Price ER, Nadeau J, and Strohl KP, J Appl Physiol 92: 1133–1140, 2002) to determine whether such differences persisted into non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. Measures assessed in C57BL/6J (B6; Jackson Laboratory) and two A/J strains (A/J Jackson and A/J Harlan) included ventilatory behavior [respiratory frequency, tidal volume, minute ventilation, mean inspiratory flow, and duty cycle (inspiratory time/total breath time)], and metabolism, as performed by the plethsmography method with animals instrumented to record EEG, electromyogram, and heart rate. In all strains, there were reductions in minute ventilation and CO2 production in NREM compared with wakefulness ( P < 0.001) and a further reduction in REM compared with NREM ( P < 0.001), but no state-by-stain interactions. Frequency showed strain ( P < 0.0001) and state-by-strain interactions ( P < 0.0001). The A/J Jackson did not change frequency in REM vs. NREM [141 ± 15 (SD) vs. 139 ± 14 breaths/min; P = 0.92], whereas, in the A/J Harlan, it was lower in REM vs. NREM (168 ± 14 vs. 179 ± 12 breaths/min; P = 0.0005), and, in the B6, it was higher in REM vs. NREM (209 ± 12 vs. 188 ± 13 breaths/min; P < 0.0001). Heart rate exhibited strain ( P = 0.003), state ( P < 0.0001), and state-by-strain interaction ( P = 0.017) and was lower in NREM sleep in the A/J Harlan ( P = 0.035) and B6 ( P < 0.0001). We conclude that genetic background affects features of breathing during NREM and REM sleep, despite broad changes in state, metabolism, and heart rate.

Ventilatory response to hypercapnia during sleep and wakefulness in cats

1984 ◽  
Vol 56 (5) ◽  
pp. 1347-1354 ◽  
Author(s):  
A. Netick ◽  
W. J. Dugger ◽  
R. A. Symmons
Keyword(s):  
Eye Movement ◽  
Response Curve ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Nrem Sleep ◽  
Rapid Eye Movement ◽  
Ventilatory Responses ◽  
A Value ◽  
The Right ◽  
Hypercapnic Response

Eucapnic breathing and ventilatory responses to hypercapnia were studied in seven cats during sleep and wakefulness. No significant differences were found in minute ventilation (VE), alveolar ventilation (VA), or alveolar PCO2 (PACO2) between wakefulness (W) and non-rapid-eye-movement (NREM) sleep, but VA and VE were less during rapid-eye-movement (REM) sleep than W, and PACO2 declined during REM compared with NREM. To test the hypercapnic response, cats were required to rebreathe from a bag containing 6% CO2 and 94% O2 (to eliminate the hypoxic response). The response curve was displaced to the right during NREM and REM; the slope was reduced only during REM to a value about 75% of W and NREM. Eye movements, quantifying phasic REM, were only slightly correlated (negatively) with the deviation of ventilation from the response curve. The hypercapnic response was diminished, not eliminated, during REM, even during phasic REM. The reduced slope arose principally from the failure of the expiratory time to shorten with hypercapnia as during W and NREM. The cat's hypercapnic response compared with the dog's, measured by others with the same methodology, suggests that differences between species may be more crucial than methodology in explaining earlier contradictory results.

Effects of selective sleep deprivation on ventilation during recovery sleep in normal humans

1992 ◽  
Vol 72 (1) ◽  
pp. 100-109 ◽  
Author(s):  
J. B. Neilly ◽  
N. B. Kribbs ◽  
G. Maislin ◽  
A. I. Pack
Keyword(s):  
Sleep Deprivation ◽  
Eye Movement ◽  
Rem Sleep ◽  
Minute Ventilation ◽  
Nrem Sleep ◽  
Rapid Eye Movement ◽  
Rem Sleep Deprivation ◽  
Sleep Period ◽  
Recovery Sleep ◽  
The Relationship

To assess the effects of selective sleep loss on ventilation during recovery sleep, we deprived 10 healthy young adult humans of rapid-eye-movement (REM) sleep for 48 h and compared ventilation measured during the recovery night with that measured during the baseline night. At a later date we repeated the study using awakenings during non-rapid-eye-movement (NREM) sleep at the same frequency as in REM sleep deprivation. Neither intervention produced significant changes in average minute ventilation during presleep wakefulness, NREM sleep, or the first REM sleep period. By contrast, both interventions resulted in an increased frequency of breaths, in which ventilation was reduced below the range for tonic REM sleep, and in an increased number of longer episodes, in which ventilation was reduced during the first REM sleep period on the recovery night. The changes after REM sleep deprivation were largely due to an increase in the duration of the REM sleep period with an increase in the total phasic activity and, to a lesser extent, to changes in the relationship between ventilatory components and phasic eye movements. The changes in ventilation after partial NREM sleep deprivation were associated with more pronounced changes in the relationship between specific ventilatory components and eye movement density, whereas no change was observed in the composition of the first REM sleep period. These findings demonstrate that sleep deprivation leads to changes in ventilation during subsequent REM sleep.

Ventilatory effects of specific carotid body hypocapnia in dogs during wakefulness and sleep

1995 ◽  
Vol 79 (3) ◽  
pp. 689-699 ◽  
Author(s):  
C. A. Smith ◽  
K. W. Saupe ◽  
K. S. Henderson ◽  
J. A. Dempsey
Keyword(s):  
Eye Movement ◽  
Carotid Body ◽  
Rem Sleep ◽  
Minute Ventilation ◽  
Control Period ◽  
Nrem Sleep ◽  
Inhibitory Effect ◽  
Rapid Eye Movement ◽  
Inspiratory Time ◽  
Ventilatory Effects

We used extracorporeal perfusion of the vascularly isolated carotid sinus region to determine the effects of specific carotid body chemoreceptor hypocapnia-alkalosis on ventilatory control in the unanesthetized dog. Eight female dogs were studied during wakefulness, non-rapid-eye-movement (NREM) sleep, and rapid eye movement (REM) sleep. Carotid body perfusions lasted from 1 to 2 min, and each trial was preceded by a 1-min control period. Two levels of carotid body hypocapnia were employed, approximately 7 and 14 Torr below eupneic levels in a given dog. We found that 1) During wakefulness and NREM sleep, carotid body hypocapnia caused reduced tidal volume (VT) but not apnea or expiratory time prolongation. 2) The inhibition of ventilation in response to carotid body hypocapnia was graded below normocapnia, showing the highest sensitivity at carotid body PCO2 near 7 Torr below eupneic values. Inhibition reached a maximum near 14 Torr below the eupneic level; VT, inspiratory minute ventilation (VI), and VT-to-inspiratory time ratio fell 31, 23, and 27% in wakefulness and 30, 23, and 30% in NREM sleep. 3) Reductions in ventilation in response to carotid body hypocapnia are lessened but still persist throughout perfusion (up to at least 130 s) despite significant systemic hypercapnia. 4) During REM sleep, carotid body hypocapnia had no consistent inhibitory effect on ventilation until carotid body PCO2 was reduced to values near 14 Torr below the eupneic level, at which point ventilation was similar to wakefulness and NREM. 5) Moderate carotid body hypocapnia was as effective as carotid body hyperoxia in reducing VT and VI. We conclude that carotid body hypocapnia-alkalosis can significantly inhibit eupneic VT and ventilation during wakefulness and NREM sleep and, if the hypocapnia is severe enough, during REM sleep.

Sleep Disorders

2015 ◽  
Author(s):  
Sudhansu Chokroverty
Keyword(s):  
Sleep Apnea ◽  
Sleep Disorders ◽  
Eye Movement ◽  
Rem Sleep ◽  
Sleep Apnea Syndrome ◽  
Nrem Sleep ◽  
Rapid Eye Movement ◽  
Circadian Rhythm Sleep Disorders ◽  
Apnea Syndrome ◽  
Sleep Mechanism

Recent research has generated an enormous fund of knowledge about the neurobiology of sleep and wakefulness. Sleeping and waking brain circuits can now be studied by sophisticated neuroimaging techniques that map different areas of the brain during different sleep states and stages. Although the exact biologic functions of sleep are not known, sleep is essential, and sleep deprivation leads to impaired attention and decreased performance. Sleep is also believed to have restorative, conservative, adaptive, thermoregulatory, and consolidative functions. This review discusses the physiology of sleep, including its two independent states, rapid eye movement (REM) and non–rapid eye movement (NREM) sleep, as well as functional neuroanatomy, physiologic changes during sleep, and circadian rhythms. The classification and diagnosis of sleep disorders are discussed generally. The diagnosis and treatment of the following disorders are described: obstructive sleep apnea syndrome, narcolepsy-cataplexy sydrome, idiopathic hypersomnia, restless legs syndrome (RLS) and periodic limb movements in sleep, circadian rhythm sleep disorders, insomnias, nocturnal frontal lobe epilepsy, and parasomnias. Sleep-related movement disorders and the relationship between sleep and psychiatric disorders are also discussed. Tables describe behavioral and physiologic characteristics of states of awareness, the international classification of sleep disorders, common sleep complaints, comorbid insomnia disorders, causes of excessive daytime somnolence, laboratory tests to assess sleep disorders, essential diagnostic criteria for RLS and Willis-Ekbom disease, and drug therapy for insomnia. Figures include polysomnographic recording showing wakefulness in an adult; stage 1, 2, and 3 NREM sleep in an adult; REM sleep in an adult; a patient with sleep apnea syndrome; a patient with Cheyne-Stokes breathing; a patient with RLS; and a patient with dream-enacting behavior; schematic sagittal section of the brainstem of the cat; schematic diagram of the McCarley-Hobson model of REM sleep mechanism; the Lu-Saper “flip-flop” model; the Luppi model to explain REM sleep mechanism; and a wrist actigraph from a man with bipolar disorder. This review contains 14 highly rendered figures, 8 tables, 115 references, and 5 MCQs.

Mechanics of the respiratory system and breathing pattern during sleep in normal humans

1984 ◽  
Vol 56 (1) ◽  
pp. 133-137 ◽  
Author(s):  
D. W. Hudgel ◽  
R. J. Martin ◽  
B. Johnson ◽  
P. Hill
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Breathing Pattern ◽  
Minute Ventilation ◽  
Transpulmonary Pressure ◽  
Dynamic Compliance ◽  
Face Mask ◽  
Esophageal Pressure ◽  
Rapid Eye Movement ◽  
Airflow Resistance

The purposes of this investigation were to describe the changes in 1) dynamic compliance of the lungs, 2) airflow resistance, and 3) breathing pattern that occur during sleep in normal adult humans. Six subjects wore a tightly fitting face mask. Flow and volume were obtained from a pneumotachograph attached to the face mask. Transpulmonary pressure was calculated as the difference between esophageal pressure obtained with a balloon and mask pressure. At least 20 consecutive breaths were analyzed for dynamic compliance, airflow resistance, and breathing pattern during wakefulness, non-rapid-eye-movement stage 2 and rapid-eye-movement (REM) sleep. Dynamic compliance did not change significantly. Airflow resistance increased during sleep; resistance was 3.93 +/- 0.56 cmH2O X 1–1 X s during wakefulness, 7.96 +/- 0.95 in stage 2 sleep, and 8.66 +/- 1.43 in REM sleep (P less than 0.02). By placing a catheter in the retroepiglottic space and thus dividing the airway into upper and lower zones, we found the increase in resistance occurred almost entirely above the larynx. Decreases in tidal volume, minute ventilation, and mean inspiratory flow observed during sleep were not statistically significant.

Sleep Disorders

2015 ◽  
Author(s):  
Sudhansu Chokroverty
Keyword(s):  
Sleep Apnea ◽  
Sleep Disorders ◽  
Eye Movement ◽  
Rem Sleep ◽  
Sleep Apnea Syndrome ◽  
Nrem Sleep ◽  
Rapid Eye Movement ◽  
Circadian Rhythm Sleep Disorders ◽  
Apnea Syndrome ◽  
Sleep Mechanism

Recent research has generated an enormous fund of knowledge about the neurobiology of sleep and wakefulness. Sleeping and waking brain circuits can now be studied by sophisticated neuroimaging techniques that map different areas of the brain during different sleep states and stages. Although the exact biologic functions of sleep are not known, sleep is essential, and sleep deprivation leads to impaired attention and decreased performance. Sleep is also believed to have restorative, conservative, adaptive, thermoregulatory, and consolidative functions. This review discusses the physiology of sleep, including its two independent states, rapid eye movement (REM) and non–rapid eye movement (NREM) sleep, as well as functional neuroanatomy, physiologic changes during sleep, and circadian rhythms. The classification and diagnosis of sleep disorders are discussed generally. The diagnosis and treatment of the following disorders are described: obstructive sleep apnea syndrome, narcolepsy-cataplexy sydrome, idiopathic hypersomnia, restless legs syndrome (RLS) and periodic limb movements in sleep, circadian rhythm sleep disorders, insomnias, nocturnal frontal lobe epilepsy, and parasomnias. Sleep-related movement disorders and the relationship between sleep and psychiatric disorders are also discussed. Tables describe behavioral and physiologic characteristics of states of awareness, the international classification of sleep disorders, common sleep complaints, comorbid insomnia disorders, causes of excessive daytime somnolence, laboratory tests to assess sleep disorders, essential diagnostic criteria for RLS and Willis-Ekbom disease, and drug therapy for insomnia. Figures include polysomnographic recording showing wakefulness in an adult; stage 1, 2, and 3 NREM sleep in an adult; REM sleep in an adult; a patient with sleep apnea syndrome; a patient with Cheyne-Stokes breathing; a patient with RLS; and a patient with dream-enacting behavior; schematic sagittal section of the brainstem of the cat; schematic diagram of the McCarley-Hobson model of REM sleep mechanism; the Lu-Saper “flip-flop” model; the Luppi model to explain REM sleep mechanism; and a wrist actigraph from a man with bipolar disorder. This review contains 14 highly rendered figures, 8 tables, 115 references, and 5 MCQs.

Arousal Characteristics in Patients with Parkinson’s Disease and Isolated Rapid Eye Movement Sleep Behavior Disorder

SLEEP ◽  
2021 ◽  
Author(s):  
Andreas Brink-Kjær ◽  
Matteo Cesari ◽  
Friederike Sixel-Döring ◽  
Brit Mollenhauer ◽  
Claudia Trenkwalder ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Eye Movement ◽  
Rem Sleep ◽  
Regression Models ◽  
Muscle Tone ◽  
Behavior Disorder ◽  
Nrem Sleep ◽  
Rapid Eye Movement ◽  
Sleep Behavior

Abstract Study objectives Patients diagnosed with isolated rapid eye movement (REM) sleep behavior disorder (iRBD) and Parkinson’s disease (PD) have altered sleep stability reflecting neurodegeneration in brainstem structures. We hypothesize that neurodegeneration alters the expression of cortical arousals in sleep. Methods We analyzed polysomnography data recorded from 88 healthy controls (HC), 22 iRBD patients, 82 de novo PD patients without RBD and 32 with RBD (PD+RBD). These patients were also investigated at a 2-year follow-up. Arousals were analyzed using a previously validated automatic system, which used a central EEG lead, electrooculography, and chin electromyography. Multiple linear regression models were fitted to compare group differences at baseline and change to follow-up for arousal index (ArI), shifts in electroencephalographic signals associated with arousals, and arousal chin muscle tone. The regression models were adjusted for known covariates affecting the nature of arousal. Results In comparison to HC, patients with iRBD and PD+RBD showed increased ArI during REM sleep and their arousals showed a significantly lower shift in α-band power at arousals and a higher muscle tone during arousals. In comparison to HC, the PD patients were characterized by a decreased ArI in NREM sleep at baseline. ArI during NREM sleep decreased further at the 2-year follow-up, although not significantly Conclusions Patients with PD and iRBD present with abnormal arousal characteristics as scored by an automated method. These abnormalities are likely to be caused by neurodegeneration of the reticular activation system due to alpha-synuclein aggregation.

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