Arterial pressure changes during spontaneous sleep in man

Coccagna, G; Mantovani, M; Brignani, F; Manzini, A; Lugaresi, E

doi:10.1016/0013-4694(71)90098-8

Cited by 184 publications

(66 citation statements)

References 8 publications

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“…This hypertensive effect of chronic intermittent hypoxia and hypercapnia has been well described previously [16,[18][19][20][21][22] and its importance stems from the clear association of OSA and systemic hypertension [23][24][25]. Systemic hypertension in the present study was not associated with left ventricular hypertrophy.…”

Section: Discussionsupporting

confidence: 55%

Chronic intermittent hypercapnic hypoxia increases pulmonary arterial pressure and haematocrit in rats

McGuire

Bradford

2001

Eur Respir J

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Chronic intermittent hypercapnic hypoxia increases pulmonary arterial pressure and haematocrit in rats. M. McGuire, A. Bradford. #ERS Journals Ltd 2001. ABSTRACT: Sleep-disordered breathing is associated with pulmonary hypertension and raised haematocrit. The multiple episodes of apnoea in this condition cause chronic intermittent hypoxia and hypercapnia but the effects of such blood gas changes on pulmonary pressure or haematocrit are unknown. The present investigation tests the hypothesis that chronic intermittent hypercapnic hypoxia causes increased pulmonary arterial pressure and erythropoiesis.Rats were treated with alternating periods of normoxia and hypercapnic hypoxia every 30 s for 8 h per day for 5 days per week for 5 weeks, as a model of the intermittent blood gas changes which occur in sleep-disordered breathing in humans. Haematocrit, red blood cell count and haemoglobin concentration were measured each week and systemic and pulmonary arterial blood pressure and heart weight were measured after 5 weeks.In relation to control, chronic intermittent hypercapnic hypoxia caused a significant increase in systemic (104.3¡4.7 mmHg versus 121.0¡10.4 mmHg) and pulmonary arterial pressure (20.7¡6.8 mmHg versus 31.3¡7.2 mmHg), right ventricular weight (expressed as ratios) and haematocrit (45.2¡1.0% versus 51.5¡1.5%).It is concluded that the pulmonary hypertension and elevated haematocrit associated with sleep-disordered breathing is caused by chronic intermittent hypercapnic hypoxia. Sleep disordered breathing affects 1-4% of adults [1]. It is associated with multiple episodes of hypoxia and hypercapnia due to hypopnoea or apnoea, which are either caused by intermittent collapse of the upper airway (UA), termed obstructive sleep apnoea (OSA; the most common form of sleep disordered breathing), or a reduced drive to breath, termed central apnoea [2]. The condition is associated with a number of cardiovascular changes, including increased pulmonary and systemic arterial blood pressure, right ventricular hypertrophy, cardiac arrhythmias and increased haematocrit. Diurnal pulmonary hypertension is present in 17-42% of OSA patients [3][4][5][6][7] and represents a serious threat to long-term outcome in these patients [8]. The cause of pulmonary hypertension in these patients is unknown. During an apnoeic event, pulmonary arterial pressure is acutely increased [9], presumably due to hypoxic pulmonary vasoconstriction, so that repetitive episodes of increased pressure may ultimately give rise to daytime pulmonary hypertension [10]. In support of this, it has recently been shown that chronic intermittent hypocapnic hypoxia in rats causes right ventricular hypertrophy, suggesting that pulmonary arterial pressure is increased [11]. However, apnoeas are accompanied by hypercapnia as well as hypoxia [12], but the effects of this combination of chronic intermittent blood gas changes on pulmonary arterial pressure are unknown. It is known that chronic continuous hypercapnia protects against the effects of continuous hypoxia...

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Section: Discussionsupporting

confidence: 55%

Chronic intermittent hypercapnic hypoxia increases pulmonary arterial pressure and haematocrit in rats

McGuire

Bradford

2001

Eur Respir J

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“…In man, a number of behavioral and neuromuscular functions have a similar cycle of occurrence. These include rapid eye movement sleep (25), dreaming and penile tumescence (26), blood pressure variations (27), telemetered gross body activity (28), oral intake activity (29), and plasma norepinephrine concentrations (30). bly unrelated, these synchronous secretory and motor events suggest the existence of a central primary oscillator to which these systems are coupled directly or indirectly.…”

Section: Discussionmentioning

confidence: 99%

Fasting enhances growth hormone secretion and amplifies the complex rhythms of growth hormone secretion in man.

K¹,

Veldhuis²,

Johnson³

et al. 1988

J. Clin. Invest.

463

219

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Studies in man have shown that the episodic release of growth hormone (GH) is infrequent and erratic, and unlike that in the rat does not appear to have discernible ultradian periodicities. However, these observations in nonfasted subjects may be invalid since mixed nutrients have unpredictable effects on GH release. Moreover, in the fed state basal GH levels are frequently undetectable, thus rendering the identification of low amplitude pulses unreliable. Accordingly, the 24-h pulsatile pattern of GH secretion obtained from repetitive venous sampling in six normal adult male subjects was examined during a control fed day and during the first and fifth days of a 5-d fast. The GH data were analyzed using two distinct methods: a discrete pulse detection algorithm (Cluster analysis) and Fourier expansion time-series, which allows fixed periodicities of secretory activity to be resolved. The 5-d fast resulted in a significant increase in discrete GH pulse frequency (5.8±0.7 vs. 9.9±0.7 pulses/24 h, P = 0.028), 24 h integrated GH concentration (2.82±0.50 vs. 8.75±0.82 g min/ml; P = 0.0002), and maximal pulse amplitude (5.9±1.1 vs. 12.3±1.6 ng/ml, P < 0.005). While multiple low-amplitude sinusoidal periodicities were present on the control fed day, time-series analysis revealed enhancement of circadian and ultradian cycles on the first and fifth days of fasting. Concomitantly, fasting resulted in a decline (day 1 vs. day 5) in serum concentrations of somatomedin C (1.31±0.22 vs. 0.77±0.18 U/ml) and glucose (4.9±0.2 vs. 3.2±0.2 mmol/liter), and a marked rise in free fatty acid (0.43±0.12 vs. 1.55±0.35 mmol/liter) and acetoacetate (35±6 vs. 507±80 nmol/liter).We conclude that the acute nutritional status is an important determinant of spontaneous pulsatile GH secretion in man. Fast-induced enhancement of GH release is achieved through combined frequency (discrete pulses) and amplitude (sinusoidal periodicities) modulation. Such alterations in somatotropic hormone release may play an important role in substrate homeostasis during starvation.

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“…It is SWS that has first priority for recovery after sleep deprivation (Berger & Oswald, 1962), SWS has been concluded to be 'worth more' (Dement & Greenberg, 1966), it is associated with the lowest degree of nocturnal responsiveness (Williams et al, 1966), it is specifically associated with the large nocturnal growth hormone secretion (Sassin et al, 1969), it is coupled with the most profound degree of rest as indicated by the lowest whole body oxygen consumption (Brebbia & Altshuler, 1968;Haskell et al, 1981) and is coupled with the lowest level of blood pressure (Coccagna et al, 1971). It may be, of -course, that trazodone merely acts upon some final generating mechanism of EEG waves, but the fact that it is associated with subjectively improved quality of sleep allows the hypothesis that the increased duration of slow-wave sleep that we have observed is correlated with a more profound degree of rest and restoration.…”

Section: Discussionmentioning

confidence: 99%

Trazodone enhances sleep in subjective quality but not in objective duration.

Montgomery¹,

Oswald²,

Morgan³

et al. 1983

Brit J Clinical Pharma

135

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1 Nine volunteer poor sleepers, of mean age 61 years, took trazodone 150 mg nightly for 3 weeks, preceded by 2 weeks and followed by 1 week of matching blanks, in order to examine the effects of electrophysiologically-recorded and subjectively-rated sleep. The second of the initial weeks of matching blanks served as a baseline week. 2 In the subjective ratings, sleep improved in quality on trazodone, significantly so in the first and second weeks of intake, though with significant rebound insomnia on the second withdrawal night. 3 Trazodone halved the frequency of arousals interrupting sleep, and it reduced the time spent in stage 1 (drowsiness). It increased the duration of slow-wave sleep (stages 3 + 4), with a negative rebound following withdrawal. It reduced the time spent in REM sleep, with a rebound above baseline levels after withdrawal. 4 Trazodone did not change total sleep duration, nor the time required to fall asleep. 5 The effects of trazodone were sustained or became enhanced during the period of intake. They persisted for over 24 h after the last dose, and rebound effects were maximal on the second withdrawal night.

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Arterial pressure changes during spontaneous sleep in man

Cited by 184 publications

References 8 publications

Chronic intermittent hypercapnic hypoxia increases pulmonary arterial pressure and haematocrit in rats

Chronic intermittent hypercapnic hypoxia increases pulmonary arterial pressure and haematocrit in rats

Fasting enhances growth hormone secretion and amplifies the complex rhythms of growth hormone secretion in man.

Trazodone enhances sleep in subjective quality but not in objective duration.

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