Neurocirculatory consequences of abrupt change in sleep state in humans

Morgan, Barbara J.; Crabtree, David C.; Puleo, Dominic S.; Badr, M. Safwan; Toiber, F.; Skatrud, James B.

doi:10.1152/jappl.1996.80.5.1627

Cited by 157 publications

(119 citation statements)

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“…In contrast, sleep by itself (i.e. the wakefulness to sleep transition) does not affect sympathetic burst latency (Hornyak et al 1991;Takeuchi et al 1994;Morgan et al 1996). Results of the present study demonstrate that during apnoeas, asphyxia per se does not cause shortening of burst latency.…”

Section: Discussioncontrasting

confidence: 42%

Arousal from sleep shortens sympathetic burst latency in humans

Xie

Skatrud

Puleo

et al. 1999

The Journal of Physiology

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Section: Discussioncontrasting

confidence: 42%

Arousal from sleep shortens sympathetic burst latency in humans

Xie

Skatrud

Puleo

et al. 1999

The Journal of Physiology

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“…Concerning the idea of synchrony and neuroeffector transmission, enhanced sympathetic synchrony (burst discharges) has been reported in humans under conditions of stress (Callister et al, 1992;Nordin and Fagius, 1995;Morgan et al, 1996;Katragadda et al, 1997), and it has been proposed that the bursts of sympathetic activity may have important consequences for neuroeffector transmission and therefore the end organ response (Sneddon and Burnstock, 1984;Sjöblom-Widfelt et al, 1990). We propose that synchrony may bring about widespread depolarization of electrotonically coupled smooth muscle in blood vessels via ATP released from sympathetic nerve endings (Morris and Gibbins, 1992).…”

Section: Functional Significance Of Synchronization Of Sympathetic Acmentioning

confidence: 89%

Sympathetic Neuronal Oscillators are Capable of Dynamic Synchronization

et al. 1999

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In this paper we show that the discharges of sympathetic neurons innervating an identified peripheral target are driven by multiple oscillators that undergo dynamic synchronization when an entraining force, central respiratory drive (CRD), is increased. Activity was recorded from postganglionic sympathetic neurons (PGNs) innervating the caudal ventral artery of the rat tail: (1) at the population level from the ventral collector nerve (VCN); and (2) from pairs of single PGNs recorded simultaneously using a focal recording technique. Autospectral analysis of VCN activity revealed a more prominent rhythmical component in the presence of CRD than in its absence, suggesting that (1) multiple oscillators drive the discharges of PGNs and (2) these oscillators can be entrained and therefore synchronized by CRD. This interpretation was supported by analysis of the firing behavior of PGN pairs. Autocorrelation and cross-correlation analysis showed that pairs were not synchronized in the absence of CRD but showed significant synchronization when CRD was enhanced. Time-evolving spectral analysis and raster plots demonstrated that the temporal stability of PGN-to-PGN and CRD-to-PGN interactions at a given level of CRD were also dynamic in nature, with stable constant phase relationships predominating as CRD was increased. This is the first reported example of dynamic synchronization in populations of single postganglionic sympathetic neurons, and we suggest that, as in sensory processing and motor control, temporal pattern coding may also be an important feature of neuronal discharges in sympathetic pathways.

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“…Although auditory stimuli have been widely used in studies investigating the autonomic response to arousal (4,10,13,33,42), it is unlike the endogenous stimuli that induce arousal at the termination of an obstructive apnea. We chose to use the auditory stimulus because occlusion alone is unlikely to induce arousal on all occasions, and it was a standardized method of rapidly inducing cortical arousal during the two conditions.…”

Section: Discussionmentioning

confidence: 99%

Occlusion of the upper airway does not augment the cardiovascular response to arousal from sleep in humans

O'Driscoll

Κostikas²,

Simonds³

et al. 2005

Journal of Applied Physiology

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The cardiovascular response to an arousal from sleep at the termination of an obstructive apnea is more than double that to a spontaneous arousal. We investigated the hypothesis that stimulation of respiratory mechanoreceptors, by inspiring against an occluded airway during an arousal from sleep, augments the accompanying cardiovascular response. Arousals (Ͼ10 s) from stage 2 sleep were induced by a 1-s auditory tone (85 dB) during a concomitant 1-s inspiratory occlusion (O) and without an occlusion [i.e., control arousal (C)] in 15 healthy men (mean Ϯ SE: age, 25 Ϯ 1 yr). Arousals were associated with a significant increase in mean arterial blood pressure (MAP) at 4 s (P Ͻ 0.001) and a significant decrease in R-R interval at 3 s (P Ͻ 0.001). However, the magnitude of the cardiovascular response was not different during C compared with O (MAP: C, 86 Ϯ 3 to 104 Ϯ 3 mmHg; O, 86 Ϯ 3 to 105 Ϯ 3 mmHg; P ϭ 0.99. R-R interval: C, 1.12 Ϯ 0.03 to 0.89 Ϯ 0.04 s; O, 1.11 Ϯ 0.02 to 0.87 Ϯ 0.02 s, P ϭ 0.99). Ventilation significantly increased during arousals under both conditions at the second breath (P Ͻ 0.001); this increase was not different between the two conditions (C: 4.40 Ϯ 0.29 to 6.76 Ϯ 0.61 l/min, O: 4.35 Ϯ 0.34 to 7.65 Ϯ 0.73 l/min; P ϭ 0.31). We conclude that stimulation of the respiratory mechanoreceptors by transient upper airway occlusion is unlikely to interact with the arousal-related autonomic outflow to augment the cardiovascular response in healthy young men. blood pressure; heart rate SPONTANEOUS AROUSAL FROM SLEEP is associated with large surges in both heart rate and blood pressure (13,42,49). In patients with obstructive sleep apnea (OSA), the surges in sympathetic activity that occur during an arousal from sleep at the termination of an apnea are more than double in size compared with a spontaneous arousal (2,29,40). Frequent cardiovascular surges in OSA have been implicated in the increased prevalence of both nocturnal and diurnal hypertension associated with OSA (37, 41). The mechanisms responsible for the augmentation of the cardiovascular response to arousal at the termination of an apnea potentially include stimulation of the chemoreceptors (hypercapnia, hypoxia), stimulation of upper airway (UA) mechanoreceptors (occlusion), stimulation of the pulmonary stretch receptors (increasing negative intrathoracic pressure, lung inflation), or arousalrelated central activation of autonomic centers. Our laboratory has previously reported in this journal that combined stimulation of the central and peripheral chemoreceptors (using hypercapnic hypoxia) does not significantly augment the cardiovascular response to arousal from sleep in healthy human subjects (39).Brief inspiratory occlusion evokes cortical activity during wakefulness (12, 15) and sleep (1, 51). Additionally, during sleep, complete airway occlusion can rapidly induce arousal, most likely as a result of afferent activity from UA mechanoreceptors to the brain stem respiratory centers (24). Altering this afferent activity, by topical anesthes...

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Neurocirculatory consequences of abrupt change in sleep state in humans

Cited by 157 publications

References 0 publications

Arousal from sleep shortens sympathetic burst latency in humans

Arousal from sleep shortens sympathetic burst latency in humans

Sympathetic Neuronal Oscillators are Capable of Dynamic Synchronization

Occlusion of the upper airway does not augment the cardiovascular response to arousal from sleep in humans

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