Sleep stage influences the hemodynamic response to obstructive apneas.

Garpestad, Erik; Ringler, J.; Parker, J A; Remsburg, S; Weiss, J. Woodrow

doi:10.1164/ajrccm.152.1.7599824

Cited by 39 publications

(20 citation statements)

References 16 publications

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“…During REMS, the arousal response to hypoxia, hypercapnia, and upper-airway stimulation is attenuated in dogs 22–24 . The arousal response to hypoxia, hypercapnia, and upper-airway stimulation is not consistently blunted during REMS in healthy humans 25–27 , but obstructive events are more common and oxygen desaturation more severe during REMS in OSA patients 28, 29 . This has been attributed to an increase in arousal threshold during REMS relative to NREMS 30 .…”

Section: Resultsmentioning

confidence: 92%

Optogenetic Stimulation of C1 and Retrotrapezoid Nucleus Neurons Causes Sleep State–Dependent Cardiorespiratory Stimulation and Arousal in Rats

2013

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C1 catecholaminergic neurons and neurons of the retrotrapezoid nucleus are integrative nodes within the brainstem network regulating cardiorespiratory reflexes elicited by hypoxia and hypercapnia, stimuli that also produce arousal from sleep. In the present study, Channelrhodopsin2 was selectively introduced into these neurons with a lentiviral vector in order to determine if their selective activation also produces arousal in sleeping rats. Sleep stages were identified from electroencephalographic and neck muscle electromyographic recordings. Breathing was measured using unrestrained whole body plethysmography and blood pressure by telemetry. During non-rapid eye movement sleep, unilateral photostimulation of the C1 region caused arousal in 83.0 ± 14.7% of trials and immediate and intense cardiorespiratory activation. Arousal during photostimulation was also observed during rapid eye movement sleep (41.9 ± 5.6% of trials), but less reliably than during non-rapid eye movement sleep. The cardiorespiratory responses elicited by photostimulation were dramatically smaller during rapid eye movement sleep than non-rapid eye movement sleep or wakefulness. Systemic alpha1-adrenoreceptor blockade reduced the cardiorespiratory effects of photostimulation, but had no effect on the arousal caused by photostimulation during non-rapid eye movement sleep. Postmortem histology showed that neurons expressing Channelrhodopsin2-mCherry were predominantly catecholaminergic (81%). These results show that selective activation of C1 and retrotrapezoid nucleus neurons produces state dependent arousal and cardiorespiratory stimulation. These neurons, which are powerfully activated by chemoreceptor stimulation, may contribute to the sleep disruption associated with obstructive sleep apnea.

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Section: Resultsmentioning

confidence: 92%

Optogenetic Stimulation of C1 and Retrotrapezoid Nucleus Neurons Causes Sleep State–Dependent Cardiorespiratory Stimulation and Arousal in Rats

2013

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“…GARPESTAD et al [23] reported that the blood pressure in REM sleep with a 78±82% Sa,O 2 level was significantly higher than that of NREM sleep at the same saturation levels [23]. These investigators also found that, in REM sleep, further desaturation with significant lengthening of obstructive apnoea was accompanied by a significantly higher postapnoeic blood pressure elevation.…”

Section: Discussionmentioning

confidence: 97%

Nocturnal blood pressure during apnoeic and ventilatory periods in patients with obstructive sleep apnoea

Tun

Okabe²,

Hida³

et al. 1999

Eur Respir J

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The exact nature of asleep blood pressure in relation to awake blood pressure is still unclear in patients with obstructive sleep apnoea. This study aimed: 1) to investigate the asleep blood pressure in both apnoeic and ventilatory periods; 2) to determine the diurnal and nocturnal factors correlated with the changes in blood pressure from apnoea to ventilatory periods during sleep.Thirty-two patients, newly diagnosed as moderate to severe obstructive sleep apnoea with a standard nocturnal polysomnography, were enrolled. The blood pressure was monitored by using the noninvasive continuous monitoring method during polysomnographic study.The mean blood pressures in ventilatory periods during nonrapid eye movement (NREM) and rapid eye movement (REM) sleep were 117.517.9 mmHg and 128.8 21.9 mmHg, and those in apnoea periods were 94.515.4 mmHg and 102.719.0 mmHg. The average blood pressure during NREM sleep (103.016.1 mmHg) was higher than the awake blood pressure (97.015.7 mmHg). The blood pressure during REM sleep was greater than that during NREM sleep. The changes in the nocturnal blood pressure from apnoea to ventilatory periods were inversely correlated with the age and nocturnal mean nadir saturation.In conclusion, patients with obstructive sleep apnoea have higher asleep blood pressure than awake blood pressure.

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“…In each patient, both before and after treatment, all apnoeic and hypopnoeic events with a BP signal free from artefacts over the whole respiratory event, and the following unoccluded ventilatory interval were considered for BP measurements. Events during which the Finapres device operated servo set-point adjustments that could affect the evaluation of BP swings were excluded; events had to be separated from an REM period by o10 min, as sleep stage may influence BP behaviour during sleep in OSA [20]. The following variables were measured: difference between highest BP after and lowest BP during the event (systolic (DPs) and diastolic (DPd) BP values, respectively), highest Sa,O 2 preceding the event, lowest Sa,O 2 following the event, and difference between these two values (DSa,O 2 ).…”

Section: Methodsmentioning

confidence: 99%

Blood pressure responsiveness to obstructive events during sleep after chronic CPAP

et al. 2003

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The aim of this study was to investigate whether chronic continuous positive airway pressure (CPAP) affects blood pressure (BP) responsiveness to obstructive events occurring on the first night of CPAP withdrawal in obstructive sleep apnoea (OSA) after chronic treatment.Thirteen male subjects with severe OSA underwent nocturnal polysomnography with beat-by-beat BP monitoring before treatment and after 4.9¡3.4 months of home CPAP (mean daily use 5.1¡1.7 h). Variations in oxyhaemoglobin saturation (DSa,O 2 ), systolic (DPs), and diastolic (DPd) BP within nonrapid eye movement apnoeas and hypopnoeas were measured on a sample of pre-and post-treatment events. In addition, a pretreatment sample was selected for DSa,O 2 to match post-treatment events.The higher the mean DSa,O 2 was in the full pretreatment sample, the more DSa,O 2 , DPs and DPd were attenuated after treatment. Mean DPs decreased from 47.3¡8.5 in the full pretreatment sample to 42.2¡6.9 in the selected pretreatment sample, to 31.5¡5.9 mmHg in the post-treatment sample. The post-treatment value differed significantly from both the pretreatment values. The corresponding values for mean DPd were 27.0¡3.5, 24.0¡3.1 and 19.6¡3.7 mmHg, with all values differing significantly from each other.Chronic continuous positive airway pressure is followed by a decrease in apnoea/ hypopnoea-related blood pressure swings, possibly secondary to both reduced severity of event-related hypoxaemia and decreased responsiveness to obstructive events secondary to chronic prevention of nocturnal intermittent hypoxaemia. Continuous positive airway pressure (CPAP) is the most effective treatment for obstructive sleep apnoea (OSA). It abolishes upper airway obstruction during sleep for as long as it is applied, but its withdrawal is promptly followed by a reappearance of obstructive sleep-disordered breathing events, although with a lesser severity than before CPAP initiation [1][2][3][4][5]. Recent trials have demonstrated the efficacy of CPAP in improving daytime somnolence [6,7]. However, other studies have shown that even a one-night withdrawal is followed by a sudden increase in sleepiness, as demonstrated by the multiple sleep latency test [3,4].The effects of CPAP on systemic blood pressure (BP) are less well understood. Despite contrasting results, most investigations demonstrate some decrease in BP after prolonged treatment [8][9][10][11][12][13]. In most studies, the effect of prolonged OSA treatment on BP was explored by comparing BP values recorded in the 24 h before CPAP initiation with those after treatment, by means of ambulatory intermittent BP monitoring [9][10][11][12][13][14][15][16]. CPAP was withdrawn in only one study [14] during BP monitoring performed after home treatment, while in most other studies CPAP was applied during the night [8,9,11,12]. Importantly, this approach may affect nocturnal results: the extent of which a nocturnal decrease in BP is due to acute rather than chronic apnoea prevention is not clear, because CPAP, applied acutely, ma...

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Sleep stage influences the hemodynamic response to obstructive apneas.

Cited by 39 publications

References 16 publications

Optogenetic Stimulation of C1 and Retrotrapezoid Nucleus Neurons Causes Sleep State–Dependent Cardiorespiratory Stimulation and Arousal in Rats

Optogenetic Stimulation of C1 and Retrotrapezoid Nucleus Neurons Causes Sleep State–Dependent Cardiorespiratory Stimulation and Arousal in Rats

Nocturnal blood pressure during apnoeic and ventilatory periods in patients with obstructive sleep apnoea

Blood pressure responsiveness to obstructive events during sleep after chronic CPAP

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