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PubMedDate not supplied

Dissociation of hypnotic-anesthetic actions of alpha 2 agonists from cyclic AMP in the rat.

alpha 2 adrenergic agonists are used clinically for their anesthetic, analgesic, and sympatholytic actions in surgical patients. All alpha 2 adrenergic receptors, when activated by alpha 2-adrenergic agonists, are able to inhibit adenylate cyclase. We have examined the alpha 2-adrenoceptor-mediated anesthetic actions of dexmedetomidine, a highly selective alpha 2-adrenergic agonist, after pretreatment of the animals with rolipram, a cyclic AMP (cAMP)-specific phosphodiesterase inhibitor, cAMP accumulation and monoamine turnover were measured in the locus coeruleus (LC) and hippocampus (HC) following administration of rolipram [275 mg/kg, intraperitoneally (IP)] and dexmedetomidine (100-500 mg/kg, IP). The hypnotic response to dexmedetomidine was also measured in these animals. In other experiments, rats were stereotactically cannulated in the LC with an indwelling catheter, and after the second day, the tail-flick analgesic response to dexmedetomidine (3.5 mg/0.2 ml LC), following rolipram (275 mg/kg, IP) pretreatment, was assessed. In the presence of elevated cAMP levels, the hypnotic, analgesic, and sympatholytic effects of dexmedetomidine persisted. These data suggest that adenylate cyclase activity does not mediate the cellular responses to alpha 2-adrenergic agonists but instead may act in concert with other alpha 2-adrenoceptor-coupled effector mechanisms to transduce the anesthetic actions of these agents.

Adrenergic alpha-2 Receptor Agonists↗
PubMed2000

Hypnotic, anticonvulsant and muscle relaxant effects of Rubus brasiliensis. Involvement of GABA(A)-system.

UNLABELLED: Rubus brasiliensis hexanic fraction induced anxiolysis in rodents, which was reversed by flumazenil, a specific GABA(A)-benzodiazepine receptor antagonist (Nogueira et al., 1998a,b). Then, we investigated if this hexanic fraction was able to induce hypnotic, anticonvulsant and muscle relaxant effects, and the involvement of GABA(A)-system. The hexanic fraction (50, 100, 150 and 300 mg/kg, vo) was administered to male Swiss mice, 30 min before the tests. Only the dose of 300 mg/kg of this fraction decreased the latency and increased sleeping time in the barbituric-hypnosis test (sodium pentobarbital, 30 mg/kg, ip), prevented the pentylenetetrazol seizures (70 mg/kg, ip) and induced muscle relaxant (inclined plane) in 100% of animals. These effects were reversed by flumazenil (3 mg/kg, ip). IN CONCLUSION: (1) R. brasiliensis hexanic fraction induced hypnotic, anticonvulsant and muscle relaxant effects, in mice, and the GABA(A)-benzodiazepine receptor may play an important role in the effects of this fraction; (2) it is strongly suggested that this fraction contains a benzodiazepine-like principle.

Animals↗
PubMed1997

Conscious sedation with combined hypnotic agents for implantation of implantable cardioverter-defibrillators.

OBJECTIVES: The objective of this study was to evaluate the feasibility, safety and efficacy of placing implantable cardioverter-defibrillators (ICDs) in the electrophysiology laboratory using conscious sedation with combined hypnotic agents and deep sedation with etomidate. BACKGROUND: Implantable cardioverter-defibrillators with transvenous leads permit the use of simplified implantation techniques similar to those used for the insertion of permanent pacemakers. However, implantation of ICDs without general anesthesia has thus far gained limited acceptance. METHODS: In 162 patients, conscious sedation during ICD placement was achieved with combined intravenous midazolam, morphine and promethazine (Phenergan). Intravenous etomidate was administered to induce deep sedation for defibrillation threshold testing. First-time implantations were in the prepectoral position (n = 142), but some patients with preexisting devices received abdominal implants (n = 20). The results were compared with those of concurrent patients (n = 56) who received prepectoral implants under propofol anesthesia administered by an attending anesthesiologist. RESULTS: The anesthetic protocol was implemented without major intraoperative complications. During deep sedation with etomidate, episodes of apnea, hypoxia or arterial hypotension requiring therapeutic intervention did not occur. During a mean (+/-SD) follow-up period of 257 +/- 140 days (median 227, range 14 to 482), there were, among the 162 patients, a total of two nonsudden cardiac deaths-one 71 days and the other 157 days after the operation. There were two nonsudden deaths in the concurrent control subjects (n = 56)-one 13 days and the other 110 days after the operation. CONCLUSIONS: Implantation of ICDs under conscious sedation with combined hypnotic agents and deep sedation with etomidate is a safe and effective procedure with low perioperative morbidity and low long-term complication rates.

Aged↗
PubMed2001

The hypnotic actions of the fatty acid amide, oleamide.

Oleamide is an endogenous fatty acid amide which can be synthesized de novo in the mammalian nervous system, and has been detected in human plasma. It accumulates in the CSF of rats after six hours of sleep deprivation and induces sleep in naive rats and mice. Inhibition of the primary catabolic enzyme of oleamide (fatty acid amide hydrolase) by trifluoromethyl-octadecenone reduces sleep latency and increases total sleep time when given centrally to rats and peripherally to mice. While the mechanism of action of oleamide is unclear, it has been demonstrated to increase the amplitude of currents gated by 5-HT2a, 5HT2c and GABAa receptors. Moreover, the action of oleamide most relevant to sleep induction involves, in part, cannabinergic pathways, as evidenced by the ability of the cannabinoid antagonist SR 141716 to inhibit the hypnotic actions of OA. Nonetheless, enhancement of cannabinergic function may not be the only mechanism by which OA alters sleep, as it can act synergistically with subthreshold doses of triazolam (0.125 microg) to reduce sleep latency. These findings raise the possibility that OA may be representative of a group of compounds which might be developed into clinically-used hypnotics, and are discussed in the context of fatty acid derivatives as modulators of neuronal function.

Animals↗
PubMed1999

Ethanol as a hypnotic in insomniacs: self administration and effects on sleep and mood.

The purpose of this study was to assess the effects of low ethanol doses on sleep and mood and to assess its reinforcing effects used as a hypnotic. Twenty healthy adults, aged 21-45 yrs, all moderate social drinkers, were studied: eleven subjects had insomnia and nine were normal sleepers, as documented by clinical polysomnography. On two sampling nights each, ethanol (0.5 g/kg) or placebo was administered before sleep in color-coded cups presented in three doses (0.2, 0.2, and 0.1 g/kg) separated by 15 min. On three subsequent nights subjects chose their preferred presleep beverage (0.2 g/kg ethanol or placebo) based on cup color and were given an opportunity for 3 additional refills (0.2 g/kg each) of the chosen beverage at 15 min intervals, yielding a total possible dose of 0.8 g/kg. Insomniacs chose ethanol 67% of nights and normals 22%. Insomniacs chose significantly more ethanol refills than normals for an average nightly dose of 0.45 g/kg and normals took significantly more placebo refills. On the sampling nights 0.5 g/kg ethanol reduced REM sleep for both groups for the 8-hr sleep period and in insomniacs increased stage 3-4 sleep and reduced stage 1 sleep during the first half of the night to the level seen in the normals. Other sleep variables were not altered in either group or halves of the night. Presleep improvements in the Profile of Mood States tension and concentration factors were also associated with ethanol administration. Thus, acutely, both sleep and mood effects appear to be associated with the reinforcing effects of ethanol as a hypnotic for insomniacs.

Adult↗
PubMed1999

The effects of benzodiazepine (triazolam), cyclopyrrolone (zopiclone) and imidazopyridine (zolpidem) hypnotics on the frequency of hippocampal theta activity and sleep structure in rats.

In order to investigate the relative efficacy and safety of zopiclone and zolpidem, we compared the effects of higher doses of zopiclone and zolpidem on the frequency of hippocampal theta activity and sleep structure with that of triazolam. Rats were divided into triazolam treatment group (1 mg/kg, 5 mg/kg), zopiclone treatment group (20 mg/kg, 100 mg/kg) and zolpidem treatment group (20 mg/kg, 100 mg/kg). Rats were injected intraperitoneally with these drugs or their vehicle. Polygraphic sleep recording and visual frequency analysis of the hippocampal EEG activity in REM sleep were carried out for 6 h after each injection. Zolpidem, unlike triazolam and zopiclone, had a much milder reducing-effect on the frequency of hippocampal theta activity and suppressing-effect on REM sleep. These results suggest that zolpidem may prove to be a safer hypnotic drug which has fewer or milder side effects than are benzodiazepine and cyclopyrrolone hypnotics.

Animals↗
PubMed1999

Xenon suppresses the hypnotic arousal in response to surgical stimulation.

STUDY OBJECTIVE: To evaluate the suppressive effects of xenon (Xe) on hypnotic arousal at skin incision. DESIGN: Prospective, randomized study. SETTING: Operating rooms at a university hospital. PATIENTS: 35 ASA physical status I and II patients presenting for elective lower abdominal surgery. INTERVENTIONS: Patients were randomly assigned to receive one of the following regimens: 1.3 minimum alveolar concentration (MAC) isoflurane, 1.3 MAC sevoflurane, 0.7 MAC Xe with 0.6 MAC sevoflurane, 1 MAC Xe with 0.3 MAC sevoflurane, or 0.7 MAC nitrous oxide (N2O) with 0.6 MAC sevoflurane (n = 7 each group). MEASUREMENTS AND MAIN RESULTS: The bispectral index (BIS) was measured at baseline, during anesthesia, and after skin incision. BIS increased significantly at skin incision from the values noted during anesthesia in the sevoflurane and N2O groups, whereas it remained stable at incision in the other three groups (mean change in BIS: 0 +/- 9 for isoflurane, 15 +/- 8 for sevoflurane, 5 +/- 6 for 0.7 MAC Xe, 4 +/- 11 for 1 MAC Xe, and 9 +/- 5 for N2O). CONCLUSIONS: Unlike N2O, Xe was able to suppress hypnotic arousal in response to surgical stimulation when administered with sevoflurane.

Abdomen↗
PubMed2003

Older adults and withdrawal from benzodiazepine hypnotics in general practice: effects on cognitive function, sleep, mood and quality of life.

BACKGROUND: Older adults are the main recipients of repeat prescriptions for benzodiazepine (BZD) hypnotics. BZDs can impair cognitive function and may not aid sleep when taken continuously for years. This study therefore aimed to determine if withdrawing from BZDs leads to changes in patients' cognitive function, quality of life, mood and sleep. METHOD: One hundred and ninety-two long-term users of BZD hypnotics, aged > or = 65 years, were identified in 25 general practices. One hundred and four who wished to withdraw were randomly allocated to one of two groups under double-blind, placebo controlled conditions: group A's BZD dose was tapered from week 1 of the trial; group B were given their usual dose for 12 weeks and then it was tapered. An additional group (C) of 35 patients who did not wish to withdraw from BZDs participated as 'continuers'. All patients were assessed at 0, 12 and 24 weeks and 50% were reassessed at 52 weeks. RESULTS: Sixty per cent of patients had taken BZDs continuously for > 10 years; 27% for > 20 years. Of all patients beginning the trial, 80% had successfully withdrawn 6 months later. There was little difference between groups A and B, but these groups differed from continuers (C) in that the performance of the withdrawers on several cognitive/psychomotor tasks showed relative improvements at 24 or 52 weeks. Withdrawers and continuers did not differ in sleep or BZD withdrawal symptoms. CONCLUSIONS: These results have clear implications for clinical practice. Withdrawal from BZDs produces some subtle cognitive advantages for older people, yet little in the way of withdrawal symptoms or emergent sleep difficulties. These findings also suggest that, taken long-term, BZDs do not aid sleep.

Affect↗
PubMed1992

High-dose methotrexate does not affect the pharmacodynamics of phenobarbital hypnotic action but decreases the central nervous system (CNS) sensitivity to pentylenetetrazol-induced maximal seizures in rats.

Chemotherapy with high-dose methotrexate (HD-MTX) is often associated with acute neurotoxicity. We determined whether the altered neuronal function after HD-MTX [such as the reduced regional cerebral metabolic glucose rate (rCMRGlc) and slow electroencephalographic pattern] affects the sensitivity of the CNS to centrally acting drugs: the depressant phenobarbital, which reduces rCMRGlc, and the analeptic agent pentylenetetrazol (PTZ), which elevates rCMRGlc. Adult male Sabra rats received an i.v. infusion of MTX, 0.51 mg/min, to induce neurotoxicity or saline solution for 24 hr. Subsequently, MTX-treated and control groups were infused in one experiment with phenobarbital until loss of the righting reflex and in the second experiment with PTZ until the onset of maximal seizures. HD-MTX did not affect the infused hypnotic dose or serum, brain, and cerebrospinal fluid concentrations of phenobarbital at the onset of anesthesia. The convulsive dose and PTZ concentrations in the serum and brain at the onset of maximal seizures were significantly higher in the HD-MTX-treated animals. These outcomes indicate that HD-MTX and the reduced rCMRGlc that follows this treatment do not contribute to the hypnotic action of phenobarbital. On the other hand, treatment with HD-MTX exhibited anticonvulsant properties as evidenced by the reduced CNS sensitivity to PTZ-induced seizures.

Animals↗
PubMed1989

Kinetics of drug action in disease states. XXXI. Effect of experimental hyperthyroidism on the hypnotic activity of a benzodiazepine (oxazepam) in rats.

This investigation was designed to determine the effect of experimental hyperthyroidism on the hypnotic activity of a benzodiazepine and on the binding characteristics of the benzodiazepine receptor complex. Rats were made hyperthyroid by subcutaneous implantation of slow release pellets containing L-thyroxine. This treatment produced the characteristic symptoms of hyperthyroidism: increased serum thyroxine concentrations, increased heart weight and body temperature, and decreased serum protein concentrations. The hyperthyroid rats and a parallel group of normal animals (with drug-free pellets implanted subcutaneously) were slowly infused intravenously with oxazepam until they lost their righting reflex. The hyperthyroid rats required a significantly larger dose of the benzodiazepine and their total serum and cerebrospinal fluid concentrations of oxazepam (but not the serum concentration of free drug and the brain concentration) at the onset of loss of the righting reflex were modestly but statistically significantly lower than those of the normal rats. The receptor density and affinity for diazepam in hyperthyroid rats were not significantly different from those of the normal animals. Hyperthyroidism apparently affects the pharmacokinetics of oxazepam but has, at best, only a small effect on the pharmacodynamics (hypnotic activity) of the drug.

Animals↗
PubMed1993

Relaxation for insomnia and hypnotic medication use in older women.

Relaxation therapy was given to 3 groups of older women (N = 57): (a) hypnotically medicated insomniacs, (b) nonhypnotically medicated insomniacs, and (c) noninsomniacs. Groups b and c were receiving antihypertensives. Self-reported sleep and medication data were collected for 1 week at pretreatment (except relaxation), posttreatment, and 6-weeks follow-up. Three relaxation sessions, a nondemanding, hybrid method, were administered with the rationale of helping insomnia or high blood pressure. Substantial sleep improvement occurred only for nonhypnotically medicated insomniacs. Substantial sleep medication reduction (47%) occurred only for hypnotically medicated insomniacs. This relaxation approach proved valuable, but the nature of the treatment effect was dependent on the medication status of the insomniac.

Aged↗
PubMed1994

Flumazenil antagonizes the central effects of zolpidem, an imidazopyridine hypnotic.

Zolpidem is a new imidazopyridine-hypnotic that selectively binds to the central omega 1-receptor subtype. A double-blind, randomized, three-way, crossover placebo-controlled study was carried out in nine healthy male volunteers to assess the possible antagonism of central nervous system--depressant effects of zolpidem by flumazenil. Subjects received zolpidem (0.21 mg/kg) or placebo, intravenously, followed 17 minutes later by flumazenil (0.04 mg/kg) or placebo. Vigilance and performance were assessed by a trained anesthetist with use of ciliary reflex, response to a verbal instruction, subjective sedation, a tracking task, and a free recall task. Zolpidem produced a clinically relevant hypnotic effect in five subjects and significantly impaired performance in all nine subjects up to 90 minutes after dosing. Flumazenil rapidly antagonized clinical sedation in the five subjects who were asleep and significantly reversed the performance decrement within 3 minutes, without any escape phenomenon. Flumazenil did not change zolpidem plasma concentrations, confirming the pharmacodynamic nature of the interaction. Flumazenil may thus be a safe and effective antidote in patients with zolpidem overdosage.

Adult↗
PubMed1999

The hypnotic effects of melatonin treatment on diurnal sleep in humans.

This study investigated the hypnotic effects of 10 mg melatonin and placebo, which were administered at 10.00 h, according to a single-blind crossover design, on an 8-h diurnal sleep from 11.00 to 19.00 h, following a full night of sleep. The subjects were six healthy male students, each of whom underwent polysomnography and rectal temperature monitoring. Melatonin treatment significantly increased total sleep time in diurnal sleep (403.2+/-SD 72.8 min and 258.5+/-118.3 min, P<0.001). As to changes in rectal temperature during diurnal sleep, however, there were no significant differences between the melatonin and placebo conditions. Thus, these results indicated that melatonin administered at 10.00 h had direct hypnotic effects on diurnal sleep.

Adult↗
PubMed2001

Characteristics of patients with hypnotic-related psychiatric disorders in the nationwide mental hospital survey.

We investigated the characteristics of patients with hypnotic-related psychiatric disorders. Subjects were 90 patients reported in the nationwide Mental Hospital Survey in 1998, who were divided into three groups according to their history of substances use. Group A (patients without history of any illicit substance use) was estimated to be the most common and core group with iatrogenic characteristics. Hypnotic use in Group B (patients with history of any illicit substance use) was recognized as one of behavioral disorders in the psychosocial context. Patients in Group C (patients with multiple-substance use and without history of any illicit substance use) showed the most serious disorders in the context of addiction. More specified treatment programs would be required considering patients' characteristics.

Adult↗
PubMed1995

[Sleep disorders--what can be done when hypnotics no longer help? Overview and case report].

We report on the case of a 45-year old female with chronic insomnia and refractory to hypnotics, who also has a - polygraphically documented - tolerance to the imidazopyridine "zolpidem". We discuss the main differential diagnosis and demonstrate a therapeutic regimen which allows a step-by-step replacement of hypnotics by sedative antidepressants. This interval replacement treatment reduces on the one hand the risk of developing a severe withdrawal syndrome. On the other hand the replacement by sedative antidepressants improves insomnia and insomnia-associated depressive symptoms. Finally, the clinical implications and rationale of a therapeutic approach with sedative antidepressants in chronic insomnia are discussed.

Antidepressive Agents↗
PubMed1988

L-tryptophan: a rational anti-depressant and a natural hypnotic?

L-tryptophan is an essential amino acid which is the metabolic precursor of serotonin. Because of the evidence that serotonin deficiency may be an aetiological factor in some sorts of affective disorder and that serotonin is important in the biochemistry of sleep, L-tryptophan has been suggested as a "rational" anti-depressant and as a "natural" hypnotic. This paper reviews the biochemistry and pharmacology of L-tryptophan as well as the literature of the clinical trials that have been conducted with it and suggests that, by itself, L-tryptophan may be useful in mild cases of depression accompanied by endogenous features and cases of bipolar disorder resistant to standard treatments. It also potentiates the monoamine oxidase inhibitors and possibly the serotonergic tricyclic drugs. L-tryptophan may improve the depressed mood of Parkinsonian patients and has a clinically useful hypnotic action. There is evidence it may be useful in organic mental disorders induced by levodopa. Dosage schedules, contraindications and complications are discussed.

Depressive Disorder↗
PubMed1984

Insomnia and its treatment. When are hypnotics justified?

Symptomatic treatment of transient insomnias is advisable, for without treatment these sleep disorders may become persistent. The drugs of choice are the benzodiazepine hypnotics, which have minimal side effects when used for short periods in properly selected patients. The three such drugs currently available in the United States differ enough in half-life, absorption rate, and potential for drug interactions that they cannot be used interchangeably. A sound selection matches the drug's characteristics with the patient's needs. Transient insomnias must be differentiated from persistent insomnias, which are more resistant to treatment. Hypnotic agents not only are more likely to be ineffective against persistent insomnias but also have greater potential for exacerbating a sleep-related breathing disorder, producing a drug-dependent insomnia, or contributing to drug misuse.

Anti-Anxiety Agents↗