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PubMedDate not supplied

[Local mechanisms of the regulatory action of Scutellaria baicalensis and ginseng extracts on the erythropoiesis after paradoxical sleep deprivation].

The influence of ginseng and skullcap (Scutellaria baicalensis) extracts on the local mechanisms of erythropoiesis control under the conditions paradoxical sleep deprivation has been studied. The regulatory action of both preparations on the bone marrow erythropoiesis is based on their ability to influence the proliferation and differentiation in erythroid cells-precursors via modulation of the functional activity of cellular hemopoiesis-inducing microenvironment elements. In particular, the drugs induce changes in the structural and functional organization of the bone marrow and in the production of short-range humoral erythropoiesis regulatory elements.

Animals↗
PubMed1982

Regulation of cerebral serotonin binding and metabolism in sleep-deprived rats.

Two different binding sites are found for serotonin binding to crude membrane fractions isolated from rat brain. After 12 h sleep deprivation (SD) the dissociation constant of the high affinity binding KD1 = 1.4 mM, remains unchanged whereas the dissociation constant, KD2, of the low affinity binding increased from 26 to 42 nM. The number of binding sites are only moderately affected. The dissociation constant of the low affinity binding, KD2, is decreased towards control values if SD is followed by 1 or 4 h sleep. As indicated by serotonin and 5-hydroxyindoleacetic acid analyses, a statistically significant increase in serotonin metabolism is found only, if SD is followed by 1 h recovery sleep.

Animals↗
PubMed2006

Spontaneous coronary dissection associated with sleep deprivation presenting with acute myocardial infarction.

Spontaneous coronary dissection is a rare cause of myocardial ischemia, myocardial infarction and sudden cardiac death. Idiopathic spontaneous coronary artery dissection (SCAD) occurs in patient without risk factors for coronary artery disease and without underlying pregnancy. We describe a case of idiopathic spontaneous coronary dissection after sleep deprivation presenting with acute myocardial infarction. A 40 year old woman presented to an emergency department with squeezing substernal chest pain lasting 1 hour following 72 h sleep deprivation due to overtime work. On admission, ECG showed no significant ST change. But the level of CK-MB and Troponin T were increased up to 77.54 ng/ml and 1.62 ng/ml, respectively. Emergent coronary angiography demonstrated a longitudinal dissection of the middle portion in the diagonal artery with TIMI III flow to the distal part of the vessel. Because the dissected vessel was too small to pass the intravascular ultrasound (IVUS) and deploy the stent, angioplasty was not performed. Under medical treatment with aspirin, clopidogrel and unfractionated heparin, conservative management was proposed; she remained free of symptom and discharged free of chest pain and in good condition.

Adult↗
PubMed1995

Effects of flumazenil on recovery sleep and hormonal secretion after sleep deprivation in male controls.

The effects of flumazenil, a benzodiazepine antagonist, on the sleep electroencephalogram (EEG) and neuroendocrine secretion in early morning recovery sleep (0500-0800 hours) following sleep deprivation (SD; 2300-0500 hours) were studied in seven healthy men. SD induced an increase in slow wave sleep (SWS), a decrease in sleep onset latency (SOL), an enhancement of EEG delta and theta power in non-rapid-eye-movement sleep, an increase in plasma human growth hormone (GH) concentration, and a decrease in plasma cortisol levels in recovery sleep (0500-0800 hours). Plasma GH, but neither plasma cortisol nor adrenocorticotrophic hormone (ACTH) concentration was attenuated during SD as compared to sleep (2300-0445 hours). The administration of flumazenil (3 x 1 mg intravenously) during recovery sleep resulted in an inhibition in SWS, an increase in stage 2 sleep, a selective reduction in delta and theta power, and a tendency to prolongation of SOL. Plasma GH concentration was decreased but plasma cortisol and ACTH remained unaffected. Since the SD-induced changes in sleep EEG and plasma GH secretion were antagonized by flumazenil, it is suggested that electrophysiological and hormonal effects of SD are mediated at least in part through GABAergic mechanisms.

Adrenocorticotropic Hormone↗
PubMed1994

The effect of REM sleep deprivation on histamine concentrations in different brain areas.

Rats were deprived of REM sleep (REMS) for 72 h with the platform method and decapitated in the morning immediately after the deprivation or in the afternoon after having been allowed 5 hours of rebound sleep. The histamine concentrations of the anterior and posterior hypothalamus, the cortex, the hippocampus and the pineal gland were measured, as well as the tele-methylhistamine concentrations of the anterior and posterior hypothalamus. Histamine concentrations were no different after REMS deprivation compared to large platform or dry cage controls, but in the anterior hypothalamus histamine levels increased during rebound sleep only in the REMS deprived rats. tele-Methylhistamine/histamine ratios were higher after 72 h of both REMS deprivation and the large platform treatment compared to dry cage controls, indicating increased histamine utilization during the platform treatment procedure.

Analysis of Variance↗
PubMed1998

Effects of sleep deprivation and user interface on complex performance: a multilevel analysis of compensatory control.

This study was carried out to test the compensatory control model, which predicts performance maintenance under stress at the expense of effort and increased selectivity. It examined the effects of sleep deprivation on performance in an automated process control task based on a simplified life support system with two types of operator control panel interface: machine centered (M-C), in which access to the system was scheduled by the computer, and human-centered (H-C), in which access was ad-lib. The task environment also permitted the analysis of changes in strategy and in subsidiary activities (alarm reaction time, prospective memory). In a 2 x 2 repeated-measures design, 16 participants carried out the task with each interface after both normal sleep and one night of sleep deprivation (SD). No effects of SD were observed on primary task performance. As predicted, SD effects were confined to strategy changes and subsidiary task impairment and occurred only under the (low control) M-C interface. Subjective effort was increased under SD, with greater increases of effort associated with high levels of performance protection. The findings provide strong evidence in favor of the compensatory control model and argue for the use of complex, multilevel tasks in the analysis of performance under stress. Actual or potential applications include the development of more sensitive performance-testing systems based on multilevel analysis of decrement, and the design of interfaces for shift work and other suboptimal work conditions.

Adult↗
PubMed1991

Subjective sleepiness ratings: the effects of sleep deprivation, circadian rhythmicity and cognitive performance.

Computerized self-report sleepiness scales were administered before and after cognitive testing in a 72-hour sleep deprivation study. The cognitive test battery was administered every 2 hours and took approximately 1-1.25 hours. Two computerized measures of subjective sleepiness were used, one a visual analog scale, the other a Hebrew version of the Stanford sleepiness scale. The results indicated that both accumulated sleep loss, circadian and ultradian (2 cycles/day) factors were significant in determining subjective estimates of sleepiness. The extent of the differences between subjective sleepiness ratings before cognitive testing and after testing was dependent upon the phase of the circadian cycle. These differences were greatest at approximately 0200-0600 hours and least around 1000 hours. A second low point occurred at 1800-2000 hours. Analysis by complex demodulation of the individual subjects' sleepiness rating curves indicated that the amount of variance accounted for by the circadian component increased significantly after cognitive testing.

Adult↗
PubMed1986

Performance and sleepiness following moderate sleep disruption and slow wave sleep deprivation.

Recent studies have shown that periodically disrupted sleep resulted in significant daytime sleepiness and performance loss in normal young adults. One study suggested that the periodicity of disturbance rather than the total number of sleep disturbances was the primary factor in causing degraded function. However, in that study, increased performance levels could have been associated with increased levels of slow wave sleep. The present study was designed to determine whether the amount of SWS rather than the periodic disruption of sleep accounts for decreased performance of Ss with disrupted sleep. Twelve normal young adults spent two 4-night periods in the laboratory. During one 4-night series, Ss were briefly aroused either following each 10 min of sleep or whenever they entered stage 3 sleep (No SWS condition). During the second series of nights, Ss were briefly aroused after each 10 min of sleep (SWS condition). In the second series, additional arousals were performed after 5-min periods (but not when Ss were in SWS) to equalize the total number of arousals in the SWS conditions with those in the No SWS condition. Total experimental arousals were equal in the disruption conditions, and the experimental manipulation was successful in reducing total SWS to infrequent epochs of stage 3 in the No SWS condition while allowing significantly more SWS in the SWS condition. In terms of sleep stages, this difference was balanced by increased stage 2 in the No SWS condition. Despite the differential occurrence of SWS, no performance, mood, or nap latency measure was different in the SWS vs.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2001

Alterations of host defence system after sleep deprivation are followed by impaired mood and psychosocial functioning.

In healthy humans, sleep deprivation (SD) has consistently been demonstrated to impair different parameters of the host defence system and of psychosocial functioning. However, the individual timing of these alterations and their possible association have remained unknown so far. We therefore investigated functional measures of the individual host defence system as well as of subjective well-being and psychosocial performance in 10 healthy male adults before and after SD, as well as after recovery sleep. In detail, we examined the number of leukocytes, granulocytes, monocytes, lymphocytes, B cells, T cells, T helper and cytotoxic T cells, natural killer (NK) cells as well as the interleukin-1 beta (IL-1 beta) release from platelets after serotonin (5-HT) stimulation. Mood and psychosocial performance (excitement, energy, ability to work and timidity) were measured by visual analogue scales. Taken together, SD induced a deterioration of both mood and ability to work, which was most prominent in the evening after SD, while the maximal alterations of the host defence system could be found twelve hours earlier, i.e., already in the morning following SD. Our findings therefore suggest an SD-induced alteration of these psychoimmune response patterns in healthy humans preceding deterioration of mood and psychosocial functioning.

Adult↗
PubMedDate not supplied

Effects of sleep deprivation on performance and EEG spectral analysis in young adults.

Nine totally sleep deprived (TSD) and nine control subjects were evaluated with a complete battery for attention and memory performance. Frontal and temporal EEGs (5 min, eyes closed) were also recorded before and after the night. TSD subjects exhibited three performance deficits: learning the Pursuit Rotor Task, implicit recall of paired words, and distractibility on the Brown-Peterson Test. Relative to evening recordings, control subjects showed decreased morning absolute powers in all electrodes for all frequencies except for Frontal delta; TSD subjects showed increased Frontal and Temporal theta and Frontal beta. These results show that motor procedural, implicit memory, and working memory are sensitive to one night of TSD, and that Frontal and Temporal theta spectral power seem to discriminate between a night with sleep from a night without.

Adult↗
PubMed1992

Paradoxical sleep deprivation increases glutamine synthetase in rat brain.

The modifications of glutamine synthetase (GS) level, an enzyme mainly located in astrocytes, were investigated in rat after paradoxical sleep deprivation and during recovery. An immunotitration method was used to evaluate the relative level of GS in brain tissue. At the end of a 24 hrs. paradoxical sleep deprivation, a significant increase in GS level was observed both in the frontoparietal cortex and the locus coeruleus area. 4 hrs. later, during recovery, the GS level returned to control level in the cortex but was lower in the locus coeruleus area.

Animals↗
PubMed1984

[Changes in paroxysmal activity, spectral characteristics of the EEG and visual evoked potentials after sleep deprivation in patients with epilepsy and syncope].

The effect of 24-hour sleep deprivation (SD) on a number of electrophysiological indices in epilepsy and syncope was studied. Specific electroencephalographic manifestations were shown to be markedly activated which is important for the differential diagnosis of epilepsy and syncope. Following SD, patients with primary generalized epilepsy exhibited an increased spectral power of the 0- and alpha-rhythms and an elevated amplitude of visual evoked potential components (beginning with the H2 component), whereas patients with secondary generalized epilepsy had an enhanced amplitude of the late components of visual evoked potentials (P4, H4). The mechanisms of the proconvulsive effect of SD are discussed.

Adult↗
PubMed2003

Effect of sleep deprivation and driving duration on the useful visual field in younger and older subjects during simulator driving.

Nine older subjects (40-51 years) and 10 younger subjects (18-30 years) took part in two one-hour driving sessions. They performed a very monotonous task during which they had to follow a vehicle either after a complete night of sleep or after one night of sleep deprivation. While driving their useful visual field was assessed by introducing signals that would appear on the whole road scene. The analysis of the data indicates that the ability to process peripheral signals deteriorates with age, driving duration and sleep deprivation. However, the effects of these three variables on the peripheral visual ability are not similar in a dual task. The driver's useful visual field changes with age and prolongation of the monotonous driving activity according to a tunnel vision phenomenon. On the other hand, a sleep debt deteriorates the useful visual field according to a general interference phenomenon. These results are discussed in terms of decrease in the level of arousal and increase of fatigue.

Adolescent↗
PubMed2002

Paradoxical sleep deprivation facilitates subsequent corticosterone response to a mild stressor in rats.

The pituitary-adrenal responsiveness to a mild stressor was assessed in rats that were deprived of paradoxical sleep (PS) and in controls that were not deprived. Animals were either individually- or group-deprived for 96 h and hormone levels were assessed at 0, 5, 20 or 60 min after a saline injection+novelty and compared with rats which were not deprived. Both types of PS deprivation resulted in elevated adrenocorticotropin levels at 0 min, which peaked at 5 min in all animals. Individually-deprived rats exhibited the highest corticosterone (CORT) levels at 0 min. Peak levels were higher and occurred earlier in PS-deprived than in control rats (5 vs. 20 min, respectively). At 20 min, CORT levels had already returned to unstressed levels in PS-deprived rats, but not in control rats. These data indicate that PS deprivation induces facilitation of the adrenocortical response to a mild stressor, but do not suggest that PS deprivation changes the negative feedback sensitivity to CORT.

Adrenocorticotropic Hormone↗
PubMed2000

Effect of noradrenergic denervation of the amygdala upon recovery after sleep deprivation in the rat.

We previously showed that the noradrenergic locus coeruleus (NA-LC) was involved in the regulatory mechanisms of the paradoxical sleep rebound following a 10 h sleep deprivation by using a systemic injection of a specific neurotoxin, N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4). Given that rebound mechanisms are mainly located in the forebrain, we planned to study the role of the forebrain structures receiving LC afferences. In this study we evaluated the involvement of noradrenergic afferences to the central nucleus of the amygdala in the sleep rebound by DSP-4 microinjections into the central nucleus of the rat amygdala. The results showed that during the first recovery day, the paradoxical sleep rebound is lower in DSP-4 treated rats (-67.28%). These findings indicate that the amygdala, through its NA afferents, contributes to the sleep rebound mechanisms.

Adrenergic Agents↗
PubMed2006

Rapid eye movement sleep deprivation selectively impairs recall of fear extinction in hippocampus-independent tasks in rats.

Previous studies have shown that rapid eye movement (REM) sleep deprivation (RSD) exerts a detrimental effect on some memory tasks. However, whether post-learning RSD impairs memory for fear extinction, an important model of inhibitory learning, remains to be elucidated. The present study examined the effects of post-extinction RSD from 0 to 6 h and 6 to 12 h on recall of fear extinction tested 24 h after extinction training. We found that RSD from 0 to 6 h significantly increased freezing when recall of extinction of cued fear was tested in the context in which rats received extinction training whereas RSD from 6 to 12 h had no effect (experiments 1 and 2, two hippocampus-independent memory tasks). RSD at either time point had no effect on freezing when recall of extinction of cued fear was tested in the context different from that in which extinction training occurred (experiment 3, a hippocampus-dependent memory task). Additionally, we observed no effect of RSD at either time point on freezing during recall test for extinction of contextual fear (experiment 4, a hippocampus-dependent memory task). These results suggest that the effects of post-extinction RSD on memory for fear extinction are complex. RSD impairs recall of fear extinction in hippocampus-independent tasks, but does not affect recall of fear extinction in hippocampus-dependent tasks. Our findings extend previous research on the effects of RSD on learning and memory and support the notion that REM sleep is involved in memory process of certain tasks.

Acoustic Stimulation↗
PubMed1985

Suppressant effect of REM sleep deprivation on neophobia in normal rats and in rats with selective DSP-4 induced damage of locus coeruleus neurons.

The influence of REM sleep deprivation (REMD) on open field behavior of normal and locus coeruleus (LC)-damaged animals was investigated under the assumption that REMD suppresses neophobia in rats. REMD (for 24 or 72 hr, water tank technique) produced marked changes in behavior of rats encountering a novel object (white cube) in the center of the open field. REMD induced an increase in activity of treated rats; latency to the object approach was shorter, the number of center entries, time spent in object exploration, frequency of ambulation and rearing were significantly higher than in controls, also defecation was nearly abolished. LC-damage (using DSP-4, a selective central noradrenergic neurotoxin) induced neophobic-like reactions manifested by significantly prolonged latency, tendency to decreased object exploration, center entries and reduction of ambulation and rearing. This "neophobic" behavior of DSP-4 rats was counteracted by REMD as well as by subchronic, but not acute treatment, with antidepressant oxaprotiline (2 X daily for 8 days, 10 mg/kg, IP). The results provide strong support for antineophobic activity of REMD. In addition, they indicate possible similarity of REMD and subchronic oxaprotiline action on neophobia-like behavior in rats with damaged LC-neurons.

Animals↗
PubMed2005

Compensatory recruitment after sleep deprivation and the relationship with performance.

This study examined the effects of total sleep deprivation (TSD) on cerebral responses to a verbal learning task with two levels of word difficulty. A total of 32 subjects were studied with functional magnetic resonance imaging (FMRI) after normal sleep and following 36 h of TSD. Cerebral responses to EASY words were identical on both nights, but several brain regions showed increased activation to HARD words following TSD compared with following a normal night of sleep (NORM). These regions included bilateral inferior frontal gyrus, bilateral dorsolateral prefrontal cortex, and bilateral inferior parietal lobe. Better free recall performance on the HARD words after TSD was related to increased cerebral responses within the left inferior and superior parietal lobes and left inferior frontal gyrus. Recall was negatively related to activation within the right inferior frontal gyrus. Overall, the findings support the predictions of the compensatory recruitment hypothesis that task demands influence both the likelihood and location of increased cerebral activation during task performance following TSD, and refine that hypothesis by identifying a specific task demand that plays a role. The performance relationships suggest increased activation may be both beneficial (compensatory) and interfere with task performance, depending on the brain regions involved.

Adult↗