Awakening Effect Research Articles

Hypoglycemia counterregulation during sleep.

In insulin-treated patients with diabetes, episodes of severe hypoglycemia often occur during sleep, which might reflect an altered counterregulation and reduced awareness. This study examined the influence of sleep on the counterregulatory response to hypoglycemia in healthy subjects. Subjects participated in two experimental conditions; statistical tests relied on within subject comparisons. University hospital sleep laboratory. 15 healthy young men. Hypoglycemia (2.8 mmol/l) was induced for 45 min by insulin infusion once during sleep and once at the same time of night while being awake. Counterregulatory hormone concentrations (epinephrine, norepinephrine, ACTH and cortisol) and sleep recordings were obtained. Differences in the hormonal responses to hypoglycemia between sleep and wake conditions remained non-significant, indicating that sleep does not exert a primary influence on the strength of counterregulation. However, the glycemic threshold for the onset of counterregulation was significantly changed during sleep: The average onset threshold for epinephrine and norepinephrine counterregulation was 3.3 +/- 0.1 mmol/l for the wake condition and 2.7 +/- 0.1 mmol/l for the sleep condition (P < 0.001). A decrease in sleep depth coincided with the onset of the counterregulatory response, with most subjects showing signs of awakening. During sleep, the organism is less sensitive to hypoglycemia. Hypoglycemia per se has an awakening effect.

Kabbalah as Sacred Psychology

Highlighting three themes from the Kabbalah, this essay explores how psychotherapy can be enhanced through the integration of spiritual teachings and practices. Beginning with an exploration of repentance in the Jewish mystical tradition, the author examines the positive effects of spiritual awakening on identity formation and psychological development. Focusing on the Kabbalah's myths of the cosmology and messianic redemption, the author shows how these mystical motifs serve as therapeutic paradigms for growth, healing and renewal.

Microdialysis and EEG in rats reveal cortical PGE2 changes during sleep and wakefulness.

Prostaglandin (PG) E2 production was assessed in freely moving rats using the technique of microdialysis in the prefrontal cortex associated with parallel cortical EEG recordings. PGE2 concentrations were 40% higher during wakefulness than during slow wave sleep. PGE2 values varied during wakefulness with a maximal increase in the middle of the stage and a drop towards lower values before the occurrence of slow wave sleep. These variations were similar to those observed previously in the rostromedial hypothalamus, where PGE2 concentration was 2.6 times lower than that in the cortex. These data document a positive correlation between cortical EEG activation and PGE2 levels. Taken together with pharmacological data on the awakening effect of centrally administered PGE2, these observations are in favor of an involvement of PGE2 in the generation of wakefulness.

Effect of frequent brief awakenings from nonREM sleep on the nonREM-REM sleep cycle.

In the framework of a selective sleep deprivation study, eight young men were repeatedly awakened during 3 nights from nonREM sleep (nonREMS). The mean number of awakenings per night was 27.4, 29.5 and 32.8. In order to avoid excessive suppression of slow wave sleep, no awakening occurred in the first nonREMS episode. Compared to baseline, cycle 2 was significantly prolonged in all 3 nights, and cycle 3 in night 3 only. However, after subtracting the waking intervals, the differences from baseline was eliminated. The results show that the mechanisms underlying sleep cycle control keep track of sleep time and disregard epochs of waking.

Awakening, Clinical Recovery, and Psychomotor Effects After Desflurane and Propofol Anesthesia

Awakening, Clinical Recovery, and Psychomotor Effects After Desflurane and Propofol Anesthesia

Nocturnal wakefulness inhibits growth hormone (GH)-releasing hormone-induced GH secretion.

Recent studies have suggested that spontaneous release of GH as well as GH secretion stimulated by exogenous GHRH are influenced by central nervous mechanisms that regulate sleep and wakefulness. Here, the effect of nocturnal wakefulness on GH secretion stimulated by i.v. administration of GHRH was examined in two experiments in healthy men. On all nights, GHRH (1 microgram/kg BW) was injected after the subjects had slept for about 2.5 h to minimize interference of endogenous release of GH during early sleep with the response to exogenous GHRH. Both experiments included a control condition to assess GH secretory responses to GHRH during undisturbed sleep and an experimental condition to assess the effect of wakefulness. In the control conditions, subjects slept throughout the night, and GHRH was administered 170 min after sleep onset. In the experimental condition of Exp I (n = 10), subjects were awakened 150 min after sleep onset and stayed awake. GHRH was given 20 min after awakening. In the experimental condition of Exp II (n = 8), subjects were awakened 30 min after GHRH treatment, which was administered 170 min after sleep onset. GHRH administrations during sleep fell into epochs of stage 2 sleep or rapid eye movement sleep. GH secretion and sleep characteristics before GHRH administrations were comparable for experimental and control conditions of both experiments. GH secretory responses were inhibited when the subject was awake at the time of GHRH administration compared to GH responses during undisturbed sleep. Awakening the subject 30 min after GHRH administration abruptly interrupted the initiated GH secretory response. The results demonstrate a profound inhibitory effect of nocturnal awakenings on GHRH-induced GH secretion. They indicate that the GH secretory response to GHRH is strongly determined by central nervous system sleep-wake activity.

The Paradoxical Anticonvulsive and Awakening Effect of High-Dose Pyridoxine Treatment for Isoniazid Intoxication-Reply

In Reply.— De' Clari raises some interesting points regarding the potential awakening effect of pyridoxine and makes an argument for pyridoxine infusions in comatose isoniazid-poisoned patients. There are two likely mechanisms by which pyridoxine may reverse isoniazid-induced coma. First, pyridoxine is a cofactor in the transamination reaction between γ-aminobutyric (GABA) and a-ketoglutaric acid—a reaction responsible for GABA degradation. 1 The second mechanism is based on de' Clari's observation of a rapid efflux of isoniazid from the peripheral to the vascular compartment. This efflux would provide a mechanism for a reduction of central nervous system isoniazid levels. By binding to isoniazid (as pyridoxine is known to do), 2 the levels of active circulating isoniazid may be reduced. It is unknown to what degree these two mechanisms are operative in reducing the depth and duration of isoniazid-induced coma. We have some concerns regarding a continuous infusion of pyridoxine for comatose patients. One

Proopiomelanocortin (POMC)-derived peptides and sleep in the rat Part 1 — Hypnogenic properties of ACTH derivatives

The sleep-wake effects of the proopiomelanocortin (POMC)-derived peptides, i.c.v. injected, are reported. Adrenocorticotropic hormone (ACTH, 1 μg) induces an awakening effect, while its two derivatives, desacetyl-α-MSH (des-α-MSH, 1 ng) and corticotropin-like intermediate lobe peptide (CLIP, 10 ng), are respectively able to increase slow wave sleep (SWS) and paradoxical sleep (PS); the hypnogenic effect of CLIP is also observed in hypophysectomized rats. Furthermore, two hypothalamic factors known to be involved in the control of POMC derivatives were also injected; MSH Inhibiting Factor (MIF) does not influence the viligance states, while Corticotropin Releasing Factor (CRF, 1 μg) increases the waking state. Finally, some preliminary results, obtained with a restraint stress and suggesting a possible interrelation between stress, sleep and POMC derivatives, are discussed.

Effects of ICV administration of neurotensin and analogs on EEG in rats.

The electroencephalographic (EEG) effects of the ICV administration of neurotensin (NT 1-13), NT 1-8 (an inactive neurotensin fragment) and D TYR-11 NT (a long-lasting analog of neurotensin) were studied in rats. In awake rats, NT 1-13 (30 micrograms) and D TYR-11 NT (10 micrograms) induced an increase of the power spectrum in the theta range activity (4-7 Hz). In rats recorded during the sleep-wakefulness cycles, NT 1-13 (10 and 30 micrograms) and D TYR-11 NT (10 micrograms) had an awakening effect and also induced an increase of latency to the first episode of the different sleep stages (intermediate stage and slow wave sleep). NT 1-8 (30 and 90 micrograms in awake rats, 10 and 90 micrograms for sleep-wakefulness cycles) was inactive in all these experiments. Thus, it seems that all these effects can be linked to neurotensin receptors; indeed only fragments which recognize receptors possess an EEG activity.

Work at sea: a study of sleep, and of circadian rhythms in physiological and psychological functions, in watchkeepers on merchant vessels. IV. Rhythms in performance and alertness.

Performance scores on both a simple detection task and a complex visual judgment task, together with subjective alertness ratings, were collected 4-hourly from 19 watchkeepers working a "4-on/8-off" routine, and from 20 dayworkers, over consecutive days of voyages on merchant ships. Adaptation of the circadian rhythms in the measures to the shifted hours of work of the three sections of the watchkeeping crews was at best only partial. These rhythms resulted in a depression of the levels of most measures during the night hours, which was exacerbated by the effects of recent awakening from sleep. It is suggested that these unwanted variations in operational effectiveness could be largely removed by replacing the 4-on/8-off watchkeeping system, with its associated "split" sleep pattern, by one which allows a single full length sleep each day. Such a system would encourage better adaptation of the rhythms; effects of recent awakening could be avoided by the provision of an adequate "waking up" period before duty begins.

The influence of continuous and intermittent traffic noise on sleep

The effects of road traffic noise on sleep were studied in the laboratory using nine young male adults (aged 20–26). The subjects were exposed to noise with different temporal characteristics: (i) continuous traffic noise of 36 dB(A) or 45 dB(A), (ii) intermittent noise of 50 truck passages with L pmax = 45 dB(A) ( L eq = 29 dB(A)) or L pmax = 55 dB(A) ( L eq = 36 dB(A)), and (iii) a combination of continuous (45 dB(A)) and intermittent ( L pmax = 55 dB(A)) traffic noise. For one noise condition (intermittent 55 dB(A)) the effect of the use of ear plugs was also studied. The intermittent noise of L pmax = 45 dB(A) caused transitions towards lighter sleep, whereas 55 dB(A) was needed to induce awakening effects. It could be shown that the probability for arousal reactions depends on the emergence of the noise peaks from the background, rather than the absolute noise peak level. Continuous traffic noise of 45 dB(A) caused REM sleep deficits, while intermittent traffic noise of L pmax = 45 dB(A) caused stage III+IV deficits. The night with ear plugs was virtually undisturbed. After nights with REM sleep deficits the subjective sleep quality was rated lower and mood was influenced adversely. For the types of exposure used in the present investigation L eq alone is not an adequate descriptor of the noise dose, relating to the sleep disturbances observed. From the present experiment, together with other existing data, it might be concluded that the WHO recommendation of L eq = 35 dB(A) is adequate, but should be supplemented with a maximum noise level, as expressed for example in L pmax or L I , that should not be exceeded.

A comparison of the inhibitory activities of iprindole and imipramine on the uptake of 5-hydroxytryptamine and noradrenaline in brain slices

Iprindole, an active antidepressant agent of the tricyclic class, was shown to be a very weak inhibitor of the uptake of noradrenaline (IC 50 = 9 × 10 −6M) and 5-HT (IC 50 = 5 × 10 −5M) in brain slices of mice in vitro , being over 100 times less active than imipramine (IC 50 = 8 × 10 −8M and 2 × 10 −7M). In vivo iprindole inhibited the uptake reactions by less than 50 % at 100 mg/kg i.p. in mice and rats, whereas imipramine produced 50 % inhibition of the uptake of noradrenaline at 10 mg/kg i.p. and of that of 5-HT at 30 mg/kg i.p. In spite of weak uptake inhibition, iprindole potentiated the awakening effect of 1-dopa in reserpinized mice. The relationship between the antidepressant action of the tricyclic agents and the inhibition of the neuronal uptake of the biogenic amines is discussed.

Some Social Aspects of New England Colonial Mortuary Art

AbstractThe spatial, temporal, and formal controls available in Colonial gravestones permit the investigation of the various social dimensions of their occurrences. Those aspects which can be studied include status, community intermarriage, the social implications of stylistic evolution, and, in the case of the cemeteries, relative importance of community as opposed to familial control of interment practices. Such studies provide an understanding of some of the social factors reflected by measurable data of the type encountered in archaeological research. This paper documents specific responses in the evolution of marker styles to the Great Awakening's effect at Boston.

The influence of imipramine on the central effects of dihydroxyphenylalanine

A study was made in animals with chronically implanted electrodes, and in acute experiments, in order to analyze the influence of imipramine (IM) on the EEG effects of dihydroxyphenylalanine (DOPA). The following results have been obtained: 1. (1) IM potentiated the awakening effect of DOPA in reserpinized cats. The EEG effects of DOPA in reserpinized cats were biphasic: (a) a marked decrease in amplitude and slight increase in frequency, (b) synchronization. IM was unable to provoke any EEG or behavioural effect of DOPA in normal cats with chronically implanted electrodes, nor to potentiate the desynchronizing action of DOPA in chronic experiments on rabbits. 2. (2) DOPA ( dl−30 mg/kg; l−10–−15 mg/kg) infused i.v. 2 hr following IM (0·5–8·0 mg/kg) in acute experiments in cats caused a marked synchronization in the EEG. This effect was noted in immobilized cats, as well as in preparations with the brain stem sectioned at various levels. This action of DOPA was accompanied by an intense mydriasis, a decrease in recruiting reaction, an intense, although transient, pressor response and an increase in heart rate. DOPA alone induced a marked desynchronization in the postpontine and rostropontine preparations, while the EEG in encéphale isolé and in gallamine-immobilized cats was not changed. DOPA applied following chlorpromazine (0·1–1·5 mg/kg) also elicited marked synchronization in encéphale isolé and cerveau isolé cats, but not in gallamineimmobilized animals with intact neuraxes. 3. (3) Phenoxybenzamine and phentolamine antagonized the rise in blood pressure and increase in heart rate, but did not noticeably influence the EEG changes and mydriasis. α-Hydrazino-α-methyl-DOPA completely prevented the autonomie effects, but had no significant influence on DOPA induced synchronization. α-Methyl-DOPA prevented both effects of DOPA. Disulfiram and propranolol did not noticeably decrease the duration of DOPA action on the EEG.

The combined use of α-methyltyrosine and threo-dihydroxyphenylserine—selective reduction of dopamine levels in the central nervous system

Dihydroxyphenylserine- α- 14C (DOPS- α- 14) is taken up into mouse brain and decarboxylated to form norepinephrine- 14C. The combined use of nontracer doses of this amino acid ( threo- or erythro-DOPS) and the tyrosine hydroxylase inhibitor, α-methyltyrosine ethyl ester, causes a 50 per cent depletion of dopamine in the central nervous system in mice while leaving norepinephrine levels unchanged. Without threo-DOPS, α-methyltyrosine depletes both norepinephrine and dopamine levels to less than one-half their normal values. dl- Threo-DOPS rapidly replenishes norepinephrine levels in reserpine-treated mice, but does not cause the awakening effect shown by l-DOPA under the same conditions. It is suggested that the reversal of the reserpine syndrome by l-DOPA is due to formation of dopamine rather than norepinephrine in the central nervous system.

A New Analeptic: 5,5-Diethyl-1,3-Oxazin-2,4-Dione (Dioxone): II. Antagonism to some C.N.S. Depressants

Abstract Dioxone (5,5-diethyl-1,3-oxazine-2,4-dione), has been found to exhibit a strong antagonistic effect to barbiturates and chlorpromazine. Given subcutaneously, dioxone significantly reduces the mortality in mice from phenobarbitone and allows an increase in the LD50 of quinalbarbitone and hexobarbitone in mice, and pentobarbitone in rats and mice, thus showing its barbiturate antagonist action both at lethal and depressant dose levels. As with leptazol and bemegride, dioxone does not show any significant effect on the depressant activity of ethanol. It has no effect on lethal doses of chlorpromazine but it has an awakening effect on mice sedated with the drug. The pharmacological actions of dioxone, suggest that its mode of action is functional, rather than at a cellular competition level.

544 Sympatholytic drugs, dopa awakening effect and enzymes

544 Sympatholytic drugs, dopa awakening effect and enzymes

薬物の中枢興奮作用とアミンオキシダーゼ活性及び脳組織呼吸に及ぼす影響について

Relationship between awakening effect and inhibitory action of amine-oxidase activity of a drug, discovered by Mann, Quastel, and Ohta, was examined systematically by the use of analeptics, such as methylpropamin, dimethylpropamin, and 2-(3, 4-methylene-dioxyphenyl) isopropylamine, and a series of other pharmaceuticals. Further examinations were made on the possibility of the use of this point as a supplementary means in the judgement of potency of awakening effect, which is difficult to be obtained from animal tests. At the same time, effect of these pharmaceutics on brain tissue respiration was tested with a rabbit. Majority of these pharmaceutics indicated inhibitory action on amine-oxidase activity in greater or lesser degree and the levorotatory compound of analeptics, which does not indicate awakening effect in human body, inhibited amine-oxidase activity, same as dextrorotatory compound. It was found that the correlationship between awakening effect and inhibition of amine-oxidase activity was exceptionally weak. At the same time, these pharmaceutics indicated weak inhibitory action on tissue respiration but there seemed to be no correlation between that and awakening effect.

The Theological Effects of the Great Awakening in New England

The Theological Effects of the Great Awakening in New England Get access Edwin S. Gaustad Edwin S. Gaustad Search for other works by this author on: Oxford Academic Google Scholar Journal of American History, Volume 40, Issue 4, March 1954, Pages 681–706, https://doi.org/10.2307/1895863 Published: 01 March 1954