Vasopressin potentiates mineralocorticoid selectivity by stimulating 11 beta hydroxysteroid deshydrogenase in rat collecting duct

Arginine vasopressin (AVP) and corticosteroid hormones are involved in sodium reabsorption regulation in the renal collecting duct. Synergy between AVP and aldosterone has been well documented, although its mechanism remains unclear. Both aldosterone and glucocorticoid hormones bind to the mineralocorticoid receptor (MR), and mineralocorticoid selectivity depends on the MR-protecting enzyme 11 beta hydroxysteroid deshydrogenase (11-HSD), which metabolizes glucocorticoids into derivatives with low affinity for MR. We have investigated whether the activity of 11-HSD could be influenced by AVP and corticosteroid hormones. This study shows that in isolated rat renal collecting ducts, AVP increases 11-HSD catalytic activity. This effect is maximal at 10(-8) M AVP (a concentration clearly above the normal physiological range of AVP concentrations) and involves the V2 receptor pathway, while activation of protein kinase C or changes in intracellular calcium are ineffective. The stimulatory effect of AVP on 11-HSD is largely reduced after adrenalectomy, and is selectively restored by infusion of aldosterone, not glucocorticoids. We conclude that this synergy between AVP and aldosterone in controlling the activity of 11-HSD is likely to play a pivotal role in resetting mineralocorticoid selectivity, and hence sodium reabsorption capacities of the renal collecting duct.     

Enhanced slow wave sleep in patients with prolactinoma

Bidirectional interactions between nocturnal hormone secretion and sleep regulation are well established. In particular, a link between PRL and rapid eye movement (REM) sleep has been hypothesized. Short-term administration of PRL and even long-term hyperprolactinemia in animals increases REM sleep. Furthermore, sleep disorders are frequent symptoms in patients with endocrine diseases. We compared the sleep electroencephalogram of seven drug-free patients with prolactinoma (mean PRL levels 1450 +/- 1810 ng/mL; range between 146 and 5106 ng/mL) with that of matched controls. The patients had secondary hypogonadism but no other endocrine abnormalities. They spent more time in slow wave sleep than the controls (79.4 +/- 54.4 min in patients vs. 36.6 +/- 23.5 min in controls, P < 0.05). REM sleep variables did not differ between the samples. Our data suggest that chronic excessive enhancement of PRL levels exerts influences on the sleep electroencephalogram in humans. Our result, which seems to be in contrast to the enhanced REM sleep under hyperprolactinemia in rats, leads to the hypothesis that both slow wave sleep and REM sleep can be stimulated by PRL. These findings are in accordance with reports of good sleep quality in patients with prolactinoma, which is in contrast to that of patients with other endocrine diseases.     

Use of dynamic two-dimensional transesophageal echocardiography for renal cell carcinoma with cavoatrial tumor thrombus

Previous investigations involving continuous blood pressure (BP) monitoring have shown an important alteration of the 24-hour BP profile in patients with obstructive sleep apnea syndrome (OSAS). We investigated the impact of REM sleep on the 24-hour BP cycle in 16 severe OSAS male patients (mean respiratory disturbance index = 66 +/- 16 events/hour of sleep), with hypertension (mean BP 162 +/- 21/105 +/- 11 mmHg World Health Organization (WHO) protocol). Two successive nights of polysomnography were performed, and arterial BP was monitored continuously during the second 24-hour period after brachial artery cannulation. During the daytime, subjects were kept awake and supine. At 3 p.m. BP was continuously monitored during quiet supine wakefulness for 20 minutes. Systolic, diastolic and mean BP and heart rate (HR) were analyzed and tabulated in mean values of 5 minute segments. Sleep/wake information were correlated with cardiovascular variables. Each uninterrupted REM sleep period was identified and comparison between the period of quiet supine wakefulness and REM sleep HR and BP values was performed. 8 OSAS patients presented a normal drop of the mean arterial BP during the nocturnal REM sleep periods compared to quiet supine wakefulness (mean value = -10.8 +/- 7.3 mmHg) ("dippers") while the other 8 subjects ("REM sleep non dippers"), revealed an elevated mean arterial BP during REM sleep (mean value = 18.9 +/- 10.9 mm Hg). The absence of the normal circadian BP dip seen during the nocturnal sleep period is considered as an indication of vascular risk. The REM sleep non dipping may play a role in this risk.     

Hormone responses to stress in patients with major burns

The responses of the plasma stress hormones corticotrophin (ACTH), vasopressin (AVP), cortisol and corticotrophin releasing hormone (CRH) have been studied in seven consecutive patients aged between 15 and 65 years who suffered from burns of 15-95% total body surface area. There was a distinct peak in AVP (up to 100 pmol/l) and ACTH levels well above the upper limit of normal in all except one patient within 24 h of burn injury. Following the initial rise, AVP and ACTH tended to fall. Plasma CRH with one exception remained within the normal range. Concurrent measurement of plasma renin activity (PRA), haemoglobin (Hb), haematocrit (Hct) and plasma sodium (Na), to assess hydration, showed that PRA was increased in all except one patient during the first 4 days of hospital admission. The correlation between ACTH and cortisol was highly significant (P < 0.001), as was the correlation between ACTH and AVP, AVP and Na, PRA and Hb, and Hct and Na. Other significant correlations were ACTH and Hct (P = 0.023), ACTH and Na (P = 0.017), AVP and Hct (P = 0.029), CRH (P = 0.018), CRH and Hb (P = 0.001). No significant correlation could be demonstrated between CRH and ACTH or AVP. Our findings suggest that AVP plays a role in the hypercortisolaemia which accompanies major burns. The possible detrimental effect of very high levels of AVP leading to progression of burn depth and reduction of skin graft take by its potent vasoconstrictive action and water retention effect (resulting in oedema) deserves further study. As AVP has the potential to reduce tissue perfusion, the possible use of antagonists in major burns merits further consideration. Persistently raised PRA levels, despite normal biochemical and haematological parameters, may indicate that volume expansion therapy may not be adequate, and that both hypovolaemia and stress may contribute to the AVP response. Stress hormone monitoring may lead to better treatment and a reduction in burn stress.     

Differences in sleep variables, blood adenosine, and body temperature between hypothyroid and euthyroid rats before and after REM sleep deprivation

Sleep deprivation causes an increase in energy expenditure in animals. Thyroid gland function has been related to metabolic function, and this may be compromised in sleep manipulations. The objectives of the present study were the following: 1) to develop a model of hypothyroid rats by surgical removal of thyroid glands without extirpation of the parathyroid; 2) to observe the sleep architecture in euthyroid (Etx) and hypothyroid (Htx) rats, both before and after rapid eye movement (REM) sleep deprivation (96 hours); 3) to challenge both groups (i.e. Etx and Htx) with REM sleep deprivation (96 hours) and then evaluate the effects on temperature; and 4) to measure the levels of adenosine and thyroid hormones in blood. One-month-old Wistar male rats (weight 90-100 g) were studied. The thyroid gland was removed, and the parathyroid glands were reimplanted within the neck muscle (Htx) under halothane anesthesia. A sham-operated group was also included (Etx). Four months later, the animals were studied according to the following protocols. Protocol 1: Animals of both groups (i.e. Etx and Htx) were implanted for sleep recordings. After a baseline polysomnography, these animals were REM sleep deprived by the platform method (96 hours). Protocol 2. An intraperitoneal temperature transducer was placed into animals of both groups under deep halothane anesthesia. They were studied at baseline, during 96 hours of REM sleep deprivation, and on the rebound period. Protocol 3: Plasma thyroid hormones [T3, T4, and thyroid-stimulating hormone (TSH)] and plasma adenosine were determined in both groups. Results of protocol 1 indicated that the main difference observed in Htx rats during the baseline sleep was an increase in delta sleep (slow-wave sleep 2) and a reduction in waking time compared with Etx animals. REM sleep rebound after 96 hours of REM sleep deprivation was similar in both groups. In protocol 2, the main finding was that Htx animals had reduced body temperature. A significant difference in body temperature between Etx and Htx animals was found mainly during lights-on period. REM sleep deprivation in the Etx group produced an increase in body temperature. Htx animals showed the opposite effect, with a reduction in body temperature during and after REM sleep deprivation. In protocol 3, the main findings were that Htx animals exhibited a significant reduction in blood thyroid hormones (T3, T4), and that they also had high levels of plasma adenosine. REM sleep deprivation produces changes in temperature regulation. The increase in body temperature during REM sleep deprivation may require thyroid integrity. Absence of the thyroid gland does not seem to influence REM sleep recovery after its deprivation. The high plasma adenosine levels found in the Htx group may explain the increase in delta sleep in this group.     

The 24-hour rhythms in plasma growth hormone, prolactin and thyroid stimulating hormone: effect of sleep deprivation

Twenty-four hour secretory rhythms of growth hormone (GH), prolactin (PRL) and thyroid stimulating hormone (TSH) were investigated in 9 normal adult men by means of serial blood sampling at 30 min intervals. The profiles of pituitary hormones were compared in 6 subjects between in normal nocturnal sleep condition and in delayed sleep condition. Plasma GH was measured with use of highly sensitive enzyme immunoassay (EIA) recently developed. Plasma TSH was also evaluated by highly sensitive time-resolved fluorometric immunoassay (TR-FIA). Time series analysis of plasma GH and PRL was performed by auto- and cross- correlation and spectral analysis. The detection limit of EIA for GH was 0.3 pg/ml and all plasma GH levels were within the detectable range of this EIA. Cross-correlation and spectral analysis suggested the presence of approximately 2-3 h rhythmicity of plasma GH. Plasma PRL appeared to have some 24-hour rhythmicity besides its sleep-dependent component. Sleep deprivation caused marked elevation of plasma TSH during night time. It is suggested that there appears two mechanisms regulating GH secretion: one has a sleep-independent and ultradian rhythm and another has a sleep-dependent rhythm.     

Ultradian pulsatility of plasma glucose and insulin secretion rate: circadian and sleep modulation

Insulin release is a complex oscillatory process with rapid pulses (10 min) superimposed on slower circhoral oscillations (50-100 min). The exact mechanism of the circhoral oscillations, which are probably in part the consequence of a negative feedback loop linking glucose and insulin secretion rate, remains unclear. Stimulatory effects of sleep on insulin secretion are achieved by an enhancement of the oscillation amplitude which could be partly mediated by GH. The different patterns observed after acute or chronic shift of sleep suggest however an interaction between sleep influence and circadian rhythmicity, as described for numerous pituitary hormones. The intra-sleep awakenings have a modulatory effect on glucose levels but no systematic relationship exists between glucose or insulin secretion rate oscillations and the REM-NREM sleep cycles. Irrespective of the mechanisms involved, sleep or GH stimulatory effects result from a modulation of the oscillation amplitude rather than of their frequency which is probably an important feature of insulin efficacy.     

An evaluative study of the short-term effects of once-daily, sustained-release theophylline on sleep in nocturnal asthmatics

OBJECTIVE: To examine the effects of once-daily, sustained-release theophylline on sleep patterns in nocturnal asthmatics. DESIGN: Double-blind, randomised, cross-over, placebocontrolled trial over 22 days. Seven-day period to establish therapeutic levels of theophylline (11.8 +/- 3 mg/l); 8-day cross-over period of 4 days' placebo or theophylline; 7-day baseline period. Electrophysiological sleep patterns, overnight bronchoconstriction and arterial O2 saturation monitored on nights 7, 11 and 15. SETTING: Sleep Laboratory, Medical School, University of the Witwatersrand. PATIENTS: Twelve volunteers who met the criteria for asthma, had previously used theophylline, were clinically stable and had a history of nocturnal awakenings caused by asthma were enrolled. OUTCOME MEASURES: Sleep-onset latency (SOL), within-sleep wakefulness (WSW), rapid eye movement sleep (REM), slow-wave sleep (SWS), peak expiratory flow rate (PEFR) and arterial oxygen saturation. RESULTS: SOL increased on theophylline--12 minutes (range 7-9 minutes) compared with placebo--6 minutes (range 3-11 minutes); WSW increased from 33 minutes (range 17-66 minutes) on placebo to 72 minutes (range 35-150 minutes) on theophylline. REM sleep was unaltered. SWS decreased in 10-12 patients, but this difference was not significant. Early morning PEFR was significantly better on theophylline in all study limbs. CONCLUSION: Our findings show that while once-daily, sustained-release theophylline improves bronchodilation in nocturnal asthmatics, it increases nocturnal wakefulness and decreases sleep efficiency during short-term treatment. This may, however, not be a long-term effect.     

Effect of bedrest on circadian rhythms of plasma renin, aldosterone, and cortisol

Previous studies of normal men after 5 d of bedrest showed that circulatory instability on head-up tilt or standing is preceded by increased plasma renin activity (PRA) at bedrest. In the present study, the circadian rhythms of PRA, aldosterone, and cortisol have been observed in five normal men on a constant diet. In ambulatory controls, PRA and aldosterone increased normally after standing. On the third morning of bedrest, PRA was higher than before, and at noon, PRA was higher than in standing controls. The nocturnal peaks of PRA resulting from episodic renin secretion during sleep were higher after bedrest. Plasma aldosterone was also increased by bedrest. The findings are compatible with the theory that intermittent beta-adrenergic nerve activity during sleep is increased after bedrest, but other factors, such as loss of body sodium and a lower plasma volume, may also be involved.     

Contributions of the pedunculopontine region to normal and altered REM sleep

The pedunculopontine (PPN) region of the upper brainstem is recognized as a critical modulator of activated behavioral states such as wakefulness and rapid eye movement (REM) sleep. The expression of REM sleep-related physiology (e.g. thalamocortical arousal, ponto-geniculate-occipital (PGO) waves, and atonia) depends upon a subpopulation of PPN neurons that release acetylcholine (ACh) to act upon muscarinic receptors (mAChRs). Serotonin's potent hyperpolarization of cholinergic PPN neurons is central to present working models of REM sleep control. A growing body of experimental evidence and clinical experience suggests that the responsiveness of the PPN region, and thereby modulation of REM sleep, involves closely adjacent glutamatergic neurons and alternate afferent neurotransmitters. Although many of these afferents are yet to be defined, dopamine-sensitive GABAergic pathways exiting the main output nuclei of the basal ganglia and adjacent forebrain nuclei appear to be the most conspicuous and the most likely to be clinically relevant. These GABAergic pathways are ideally sited to modulate the physiologic hallmarks of REM sleep differentially (e.g. atonia versus cortical activation), because each originates from a functionally unique forebrain circuit and terminates in a unique pattern upon brain stem neurons with unique membrane characteristics. Evidence is reviewed that changes in the quality, timing, and quantity of REM sleep that characterize narcolepsy, REM sleep behavior disorder, and neurodegenerative and affective disorders (depression and schizophrenia) reflect 1) changes in responsiveness of cells in the PPN region governed by these afferents; 2) increase or decrease in PPN cell number; or 3) mAChRs mediating increased responsiveness to ACh derived from the PPN. Auditory evoked potentials and acoustic startle responses provide means independent from recording sleep to assess pathophysiologies affecting the PPN and its connections and thereby complement investigations of their role in affecting daytime functions (e.g. arousal and attention).     

Dynamical properties of the sleep EEG in different frequency bands

The information concerning the dynamic behavior of the sleep process gained by the usual evaluation of sleep EEGs according to the criteria of Rechtschaffen and Kales is limited. Therefore a new methodical approach is presented, which is a special case of spectral analyzed data processing. After digital band-pass filtering of the sleep EEG the root-mean-square (RMS) value of successive 20 s EEG epochs is calculated in defined frequency ranges. This procedure ensures to take into account the influence of the phase relation between different frequency components. The temporal course of these RMS values during the night reveals smooth curves with continuous transitions between different sleep states. In all frequency bands slow oscillations according to the sleep cycles are observable. Whereas the slow frequency bands have a temporal course with local maxima during non-REM and local minima during REM sleep, the fast frequency bands beta and gamma show the opposite behavior revealing higher RMS values during REM sleep. The relationship between the activities in different frequency bands is evaluated calculating the cross correlation coefficient. Taken together the procedure allows an objective and automated quantitative analysis of the sleep EEG. The main advantage of this approach is the characterization of the sleep cycle as a dynamic and continuous process. Compared to the classical analysis it provides a more detailed analysis of the sleep process, especially concerning the dynamics and microstructure of sleep.     

Spectral analysis in cyclic changes of human sleep evaluation

In this study cyclic changes of human sleep structure were examined. For whole-night polysomnograms of 35 healthy volunteers of both sexes, manual hypnograms were created and divided into NREM-REM cycles. EEG signals from C3-A2 derivation were analysed by computer using a Fast Fourier Transform (FFT). For consecutive NREM-REM cycles of individual sleep stages, EEG power density contents for delta, theta, alpha, sigma and beta waves were analysed. For consecutive sleep cycles, a clear decrease in NREM sleep duration, especially slow wave sleep duration, was obtained. In addition, a decrease in power density of delta waves was observed. For consecutive sleep cycles, increases in REM sleep duration and in power density of theta and alpha waves were obtained. In consecutive sleep cycles, high amplitude delta slow waves are replaced by higher frequency and lower amplitude waves. Thus stages of NREM sleep are replaced by stages of REM.     

Effects of hormones on sleep

Administration of hormones to humans and animals results in specific effects on the sleep electroencephalogram (EEG) and nocturnal hormone secretion. Studies with pulsatile administration of various neuropeptides in young and old normal controls and in patients with depression suggest they play a key role in sleep-endocrine regulation. Growth hormone (GH)-releasing hormone (GHRH) stimulates GH and slow wave sleep (SWS) and inhibits cortisol, whereas corticotropin-releasing hormone (CRH) exerts opposite effects. Changes in the GHRH:CRH ratio contribute to sleep-endocrine aberrations during normal ageing and acute depression. In addition, galanin and neuropeptide Y promote sleep, whereas, in the elderly, somatostatin impairs sleep. The rapid eye movement (REM)-nonREM cycle is modulated by vasoactive intestinal polypeptide. Cortisol stimulates SWS and GH, probably by feedback inhibition of CRH. Neuroactive steroids exert specific effects on the sleep EEG, which can be explained by gamma-aminobutyric acid(A) receptor modulation.     

Biorhythmic variations in consciousness and psychological functions.

Research indicates that indices of conscious awareness of external and internal events exhibit both ultradian approximately 90-100 min (in adulthood) and circadian 24-hr variations. The phylogenetically older ultradian rhythm represents the basic rest-activity cycle (BRAC) of N. Kleitman (1963), is continuous, and appears to contain alternation of mental activity of thought-like and fantasy type at this periodicity in wakefulness and in NREM and REM sleep. This suggests continuous cyclic alternation of relative predominance of the left and right hemispheres inherent in the BRAC. Superimposed circadian fluctuations of consciousness in a diurnally active adult typically show lowest levels in the 1st hrs after usual sleep onset and a later dip at about 5-6:00 AM if the person remains awake. After a night of sleep, daytime consciousness and performance improve in the morning, usually show an early afternoon "post-lunch dip," a sustained increase in the late afternoon and early evening, and a decrease before sleep onset. It is postulated that cortical, mainly prefrontal, hyperpolarization in NREM sleep resets the cortex for renewed high-level perceptual awareness the next day. Consciousness is not a static attribute but shows definite biorhythmic fluctuations in level and type. (French abstract) (41/2 p ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

REM sleep behaviour disorder: an overview

REM sleep behaviour disorder (RSBD) is a recently described parasomnia characterised by a history of excessive nocturnal motor activity and absence of muscle atonia during REM sleep. Only limited literature is available on this condition. The exact prevalence is unclear, but recent studies suggest it might not be an uncommon condition. The elderly are more often affected and there is a male preponderance. While transient RSBD can be seen after taking certain drugs or during drug withdrawal, the chronic type is usually idiopathic or associated with an underlying degenerative neurological condition. It can result in considerable distress and/or serious injury to the patients or their bed partners. Differential diagnoses include sleep-walking, night terrors, nightmares, nocturnal seizures, obstructive sleep apnoea, post-traumatic stress disorder, dissociative states and nocturnal confusional states. The dramatic response to clonazepam highlights the importance of recognition and appropriate treatment of this sleep disorder.     

Acute von Willebrand factor secretion from the endothelium in vivo: assessment through plasma propeptide (vWf:AgII) Levels

STUDY OBJECTIVES: Patients with coronary heart disease (CHD) and obstructive sleep apnea may have an increased cardiac risk due to nocturnal myocardial ischemia triggered by apnea-associated oxygen desaturation. Sleep structure in patients with obstructive sleep apnea is fragmented by activation of the central nervous system (CNS) (arousal) due to obstructive apneas. Nocturnal myocardial ischemia may lead to activation of the CNS as well. PATIENTS: Fourteen patients with obstructive sleep apnea and CHD disease and seven patients suffering from obstructive sleep apnea without CHD were studied. Overnight sleep studies and simultaneous six-lead ECG recordings were performed. In addition, sleep studies and ECG recordings were performed with administration of a sustained-release nitrate in these patients in a double-blinded crossover design. RESULTS: Analysis of three nights' recordings revealed 144 episodes of nocturnal myocardial ischemia in six subjects. Five patients had underlying CHD and one patient exhibited diffuse wall defects of the coronary arteries; also, 85.4% of ischemic episodes were concomitant with apneas and oxygen desaturation > 3%, and 77.8% of ischemic episodes occurred during rapid eye movement (REM) sleep, although total amount of REM sleep was only 18% of total sleep time. Mean oxygen saturation was significantly lower (p < 0.05) during apnea-associated ischemic episodes than during nonapnea-associated ischemia (77.3% vs 93.1%). Nitrate administration did not reduce ischemic episodes. Sleep architecture (macrostructure) exhibited a reduction in sleep stages non-REM 3 and 4 and REM sleep. Comparing the microstructure of sleep (arousals) within episodes with and without ischemia but similar criteria like sleep stage, apnea activity, and oxygen saturation, we found significantly more (p < 0.01) and severe (p < 0.001) arousals during periods with myocardial ischemia than during control episodes. In addition, microstructure of sleep was disturbed by myocardial ischemia itself in absence of apneas. CONCLUSION: It is concluded that patients with CHD and obstructive sleep apnea are endangered by apnea-associated ischemia and that these ischemic episodes lead to activation of the CNS and additional fragmentation of sleep. Patients with nocturnal ischemia should be screened for underlying sleep apnea even if nitrate therapy fails.     

A mucosa-associated lymphoid tissue (MALT) type lymphoma (marginal zone B-cell lymphoma) from the palatine tonsil

We studied basic sleep changes in pregnant rats in order to understand how pregnancy alters sleep. In the rat, pregnancy increased nocturnal nonREM sleep across the entire period but increased REM sleep only in the early period. By the end of pregnancy, diurnal sleep was decreased, showing that pregnancy in rats causes biphasic sleep changes as it does in humans. Termination of pregnancy returned the enhanced sleep to baseline as in the estrous cycle. Therefore, significant changes in the pattern of sleep occurred during pregnancy in rats, suggesting that the animal model may contribute to understanding the mechanism of sleep disorders related to human pregnancy.     

Sleep and stress in man: an approach through exercise and exposure to extreme environments

In this paper, the effects of exercise on human sleep (in temperate, cold, and hot climates) are compared with those of exposure to extreme environments (tropical, polar climates). Exercise has two effect: (i) when the exercise load is too heavy or if the subject is not trained to the exercise conditions, the hypothalamo-pituitary-adrenocortical axis (HPA) is strongly activated (somatic stress reaction), and a diachronic (delayed) decrease in total sleep time and slow-wave sleep (SWS) occurs with a synchronic (concomitant) sleep disruption (such as a decrease in REM sleep); (ii) a diachronic enhancement of SWS and (or) REM sleep occurs during moderate training and in athletes, with a moderate HPA activation (neurogenic stress reaction). Heat acclimatization (neurogenic stress response) results in a diachronic increase in SWS, contrary to acute heat exposure (somatic stress) which leads to a diachronic decrease in SWS. Nocturnal cold exposure (somatic and (or) neurogenic stress) provokes a synchronic decrease in REM sleep with an activation of stress hormones, which are reduced by previous acclimation (neurogenic pathway); SWS remains undisturbed in the cold, as it occurs at the beginning of the night before body cooling. In conclusion, when the brain can deal with the stressor (neurogenic stress), diachronic increases in SWS and (or) REM sleep occur. When these "central" mechanisms are overloaded, the classical "somatic" stress reaction occurs with diachronic and synchronic disruptions of the sleep structure.     

REM sleep in depressed patients: different attempts to achieve adaptation

Twenty-seven depressed patients and 10 healthy subjects were investigated in the sleep laboratory during two to three consecutive nights. Eleven of the 27 patients demonstrated the "first night effect" (group I) and 11 other patients demonstrated a clear absence of the "first night effect" (group II). Five of the 27 depressed patients were omitted from the study because they did not fit criteria for first night effect. The 10 healthy controls demonstrated a first night effect. In group I, the duration of the first rapid eye movement (REM) sleep episode was increased on the first night and on the second night the REM sleep latency was decreased, whereas REM sleep duration and eye movement (EM) density was increased. The number of the short sleep cycles (less than 40 minutes) was greater in group I versus group II and the percentage of slow-wave sleep (SWS) was also higher in group I. In depressed patients with the "first night effect" the enhanced REM sleep requirement is satisfied not only by an increased REM sleep duration but also by the improved REM sleep quality that is crucial for adaptation. The adaptive role of the increased first REM period and the increased EM density in this period is very limited.     

Precise measurement of individual rapid eye movements in REM sleep of humans

An automated analyzer for individual eye movements (EMs) has been developed that enables precise analyses of their incidence. Three new parameters for each EM are obtained: EM magnitude, the angle and speed of eyeball rotation, and the energy of each EM. All rapid eye movement (REM) sleep EMs from 40 nights of polysomnography for 20 healthy young men were analyzed. The mean frequency of eye movement (EM frequency) was 15.9 per minute. Compared to conventionally analyzed rapid eye movement (REM) density, EM frequency was more sensitive to differences among sleep cycles, nights, and individuals. The mean EM rotation was 6.27 +/- 0.021 degrees, the mean speed of rotation was 58.73 +/- 0.18 degrees/second, and mean energy was 525.85 +/- 3.82 degrees2/second. The distribution of changes in these new parameters differed from conventional measures across REM episodes. The conventional measures, REM episode duration, and REM density increased progressively in successive REM episodes in an ascent-to-right pattern. However, the new parameters peaked in the second, followed by relatively low values, producing an inverted V pattern. This discrepancy could indicate physiological mechanisms of EM that are not revealed in conventional measures of REM sleep intensity.