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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pharmacological activities of delta9-THC [(minus)-delta9-trans-tetrahydrocannabinol], CBN (Cannabinol) and mixtures of delta9-THC + CBN were studied in rabbits, rats and mice. CBN, although in general less active, mimicked the effects of delta9-THC in several pharmacological tests: corneal arreflexia in rabbits; climbing rope, open-field, irritability and aggressiveness after REM sleep deprivation in rats; catatonia, analgesia and sleeping time in mice. When the mixture delta9-THC + CBN was used, a synergistic effect occurred on most of the depressant effects. On the other hand CBN did not interfere with or slightly inhibited the excitatory effects of delta9-THC. In the one peripheral test used, CBN did not alter the delta9-THC effect.
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PMID:Pharmacologic interaction between cannabinol and delta9-tetrahydrocannabinol. 16 4

Both the MAO-B inhibitor deprenyl (2.5-10 mg/kg, ip, 60 min prior) and the MAO-B substrate beta-phenylethylamine (PEA, 40 micrograms, icv) potentiated the analgesic action of the enkephalinase inhibitor phosphoramidon (250 micrograms, icv) in animals allowed normal sleep. The enhancing effect of PEA on phosphoramidon analgesia was further potentiated by deprenyl (5 mg/kg, ip) pretreatment. Deprenyl (5 mg/kg, ip) or PEA (40 micrograms, iv) given alone did not induce analgesia in animals allowed undisturbed sleep. REM sleep deprivation (REMSD) decreased the basal pain threshold and abolished the analgesic effect of phosphoramidon. The administration of deprenyl and/or PEA failed to restore the analgesic effect of phosphoramidon in REM sleep deprived animals. The results indicate that excess PEA has a stimulatory effect on the analgesic activity of endogenously released enkephalins in rats allowed undisturbed sleep but not in REM sleep deprived animals. It is suggested that the failure of phosphoramidon to induce analgesia after REMSD, is probably due to a functional insufficiency of an enkephalinergic system.
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PMID:An analgesic effect of enkephalinase inhibition is modulated by monoamine oxidase-B and REM sleep deprivations. 309 Apr 52

Microinjections of morphine in optimal doses into the medial thalamus (40 micrograms) and periaqueductal gray matter (10-20 micrograms) produce slow-wave sleep with abondant spindles, in addition to analgesia. Like analgesia, the sleep-inducing effect is blocked by naloxone (1 mg/kg i.v., 160 micrograms i.c.). One may therefore conclude that the effect is related to the agonistic action of morphine on endorphine receptors. It is thus probable that the endorphins constitute a regulatory system acting on the medullary-thalamic sleep-inducing structures which generate the sleep spindles. At higher dose levels, injections of morphine into the same structures produce behavioral agitation resembling the dissociated REM sleep described by Jouvet and which is not blocked by naloxone. The agitation might be due to an indirect action of morphine, and therefore of endorphin receptors, acting on monoaminergic structures.
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PMID:[Opiate receptors and sleep. Effects of microinjections of morphine in the median thalamus and the periaqueductal gray matter of the rabbit (author's transl)]. 624 66

Rats treated with phosphoramidon (an enkephalinase-inhibitor 250 micrograms, i.c.v.), morphine (20 micrograms i.c.v.) or subjected to cold-water-swim (CWS, animals forced to swim in water at 5 degrees C for 5 min) showed consistent analgesia. The antinociceptive effect of phosphoramidon, morphine and CWS was antagonised by REM sleep deprivation (REMSD). It is suggested that normal duration of REM sleep is of importance for the anti-nociceptive activity of endogenous and exogenous opiates.
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PMID:REM sleep deprivation decreases the antinociceptive property of enkephalinase-inhibition, morphine and cold-water-swim. 637 76

Based on a case report, we offer brief guidelines on the perioperative management of patients with Sleep-Apnea-Syndrome (SAS) who present with a high incidence of a difficult airway and a high risk of respiratory depression during the perioperative period. A 39 year old male patient with a body mass index of 34.22 kg/m2 and receiving continuous-positive-airway-pressure-(CPAP) therapy for known SAS was scheduled for elective plastic surgery. After induction of anaesthesia and direct laryngoscopy no adequate airway could be established and the patient became hypoxic, hypercapnic and developed hypotension and bradycardia. With the use of a laryngeal mask airway the patient was stabilized and did not show neurologic sequale after immediate awakening. The following fiberoptic intubation of the awake patient, still showing tendency of upper airway obstruction, confirmed the difficult anatomical structures. The subsequent general anesthesia was uneventful. The patient received CPAP therapy and was monitored during the first postoperative night in the Intensive Care Unit. He made an uneventful recovery. He was advised to have regional anaesthesia or planned fiberoptic intubation, where possible, in the case of further anesthetic intervention. SAS has major implications for the anaesthesiologist and whenever patients exhibiting the high risk factors (obesity, male sex, history of intense snoring, impaired daytime performance, nonrefreshing daytime naps) are presented for surgery this condition should be considered. Elective surgery should be postponed until after adequate examination and treatment when necessary. Patients with SAS should always be suspected of having cardiopulmonary dysfunctions such as hypertension, cardiac dysrhythmia or cor pulmonale. It is most important to avoid sedative premedication, to initiate CPAP therapy preoperatively, to encourage regional anaesthesia if possible and to ensure close monitoring over the complete perioperative period. Planned fiberoptic intubation, preferably with surgical personnel available for an emergency airway, is a safe method for the induction of anaesthesia. Postoperatively, patients are at high risk from respiratory depression, even in the awake state. Postoperative opioid analgesia, no matter what route, should only be given under close monitoring. Independently of regional or general anaesthesia there is an increased risk of respiratory depression in the middle of the first postoperative week, suspected to be caused by the catching up on lost REM-sleep, due to shifts in the normal sleep pattern during the first postoperative days.
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PMID:[Induction of anesthesia for a patient with sleep apnea syndrome]. 1084 May 41

This study examined the effects of acute and chronic desipramine, 24-h total sleep deprivation (TSD) and 96-h REM sleep deprivation (REMSD) on physostigmine-induced hypothermia, analgesia and behaviour. The effects of acute and chronic desipramine treatment on oxotremorine-induced hypothermia were also examined. Intraperitoneal administration of physostigmine (0.5 mg/kg i.p.) induced hypothermia, analgesia, purposeless chewing movements (chewing) and head tremors. While atropine given in a low dose (1.0 mg/kg i.p. 15 min prior) did not antagonize the hypothermia, chewing and head tremor associated with physostigmine (0.5 mg/kg i.p.), a higher dose of atropine (10 mg/kg i.p. 15 min prior) decreased physostigmine-induced hypothermia, chewing and head tremor behaviour. Chronic (10 or 20 mg/kg i.p. daily for 10 days and withdrawn 24 h prior, chronic DMI) and acute (10 mg/kg, i.p. + 60 min prior, acute DMI) desipramine treatments abolished physostigmine (0.5 mg/kg i.p.)-induced hypothermia compared with saline pretreatment. Interestingly atropine (1 mg/kg i.p. 15 min prior) reversed the inhibitory effect of chronic DMI on hypothermia induced by physostigmine. Acute but not chronic DMI decreased physostigmine-induced chewing and head tremor behaviour. Atropine (1 mg/kg i.p. 15 min prior) increased the inhibitory action of acute DMI on physostigmine-induced chewing behaviour. Acute DMI (10 mg/kg i.p.) decreased oxotremorine (0.1 mg/kg i.p.)-induced hypothermia, while chronic DMI increased the hypothermic effect of oxotremorine. TSD and REMSD did not alter physostigmine (0.5 mg/kg i.p.)-induced hypothermia; however, REMSD and stress decreased physostigmine-induced analgesia and chewing.It is suggested that chronic desipramine treatment decreased physostigmine-induced hypothermia by causing hypersensitivity of pre-synaptic muscarinic receptors, whereas acute desipramine decreased the sensitivity of post-synaptic muscarinic receptors
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PMID:Functional reactivity of central cholinergic systems following desipramine treatments and sleep deprivation. 1368 87

There are many case reports of serious complications and death among obstructive sleep apnea patients (OSA) during general anesthesia or postoperative analgesia. Sedatives and anesthetic agents, pharyngeal anatomy of these patients, opiates given for analgesia, and post operative REM sleep rebound represent potential hazards for general anesthesia in OSA patients. Ideally these patients should be treated with continuous positive airway pressure (CPAP) during premedication, directly after extubation and during postoperative analgesia. Unfortunately, only about 20% of these patients are diagnosed before surgery. A special attention should be given to the symptoms and signs suggestive of OSA during preoperative visits. Screening tests should be performed in patients with suspected OSA and, if positive, a treatment should be initiated.
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PMID:[Obstructive sleep apnea: a risk for general anesthesia?]. 1815 1

Originally, a role for sleep in learning and memory has been advocated following the observation of sleep-dependent performance enhancements at simple procedural tasks. With the investigation of a variety of cognitive and behavioral abilities, multiple stages of memory were further suggested to benefit from the off-line reprocessing believed to occur during specific sleep stages. In particular, REM sleep has been implicated in the integration of new information into associative networks as well as in the abstraction and generalization of implicit rules allowing adaptive behaviors. In a recent study, we extended these observations by demonstrating that the mediating effect of expectation on placebo-induced analgesia is strengthened by sleep, and that the individual amount of REM sleep is predictive of the relief expected on the next morning. However, this relation is strongly modulated by the level of concordance between expectations and sensory information available prior to sleep. As placebo responses derive from the learned association between contextual cues and subsequent relief, these results are discussed in relation to the proposed roles of REM sleep in the integrative stages of memory processing. In light of the responsiveness of REM sleep to waking events, its expression is also proposed to reflect the cognitive demand associated with the offline reprocessing of information necessary for the assimilation of new expectations to one's belief system.
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PMID:Relief expectation and sleep. 2128 Apr 56

Placing a patient in a state of general anesthesia is crucial for safely and humanely performing most surgical and many nonsurgical procedures. How anesthetic drugs create the state of general anesthesia is considered a major mystery of modern medicine. Unconsciousness, induced by altered arousal and/or cognition, is perhaps the most fascinating behavioral state of general anesthesia. We perform a systems neuroscience analysis of the altered arousal states induced by five classes of intravenous anesthetics by relating their behavioral and physiological features to the molecular targets and neural circuits at which these drugs are purported to act. The altered states of arousal are sedation-unconsciousness, sedation-analgesia, dissociative anesthesia, pharmacologic non-REM sleep, and neuroleptic anesthesia. Each altered arousal state results from the anesthetic drugs acting at multiple targets in the central nervous system. Our analysis shows that general anesthesia is less mysterious than currently believed.
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PMID:General anesthesia and altered states of arousal: a systems neuroscience analysis. 2151 54

The gamma-aminobutyric acid type B (GABAB) receptor agonist, the sodium salt of gamma-hydroxybutyrate (GHB), significantly improved pain, sleep disturbance and fatigue in fibromyalgia (FM) patients. However, the use of GABAB receptor agonists is limited by their undesirable side-effects. To clarify whether GABAB receptor positive allosteric modulator (PAM) approach would achieve analgesia with less side-effects than GABAB receptor agonist in FM, we investigated the potential of a novel GABAB receptor PAM, ASP8062, for FM treatment. We examined the in vitro profiles of ASP8062, the effects of a GABAB receptor PAM and an agonist on pain in a rat model of FM, and the sleep/wake cycle, EEG during sleep stages and motor coordination in rats. ASP8062 showed PAM activity on human and rat GABAB receptors. Oral administration of ASP8062 significantly reversed the decrease in muscle pressure threshold in reserpine-induced myalgia rats. The analgesic effects of ASP8062 were significantly blocked by a GABAB receptor antagonist. ASP8062 had a significant effect on motor coordination at a 1000-fold higher dose than the analgesic dose in rats. ASP8062 significantly decreased total REM sleep time and frequency of sleep interruptions, and increased the power in delta waves frequency during non-REM sleep in rats. ASP8062, a novel GABAB receptor PAM, has therapeutic potential to exert analgesic effects with less side-effects compared to GABAB receptor agonists in patients with FM.
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PMID:A novel GABAB receptor positive allosteric modulator, ASP8062, exerts analgesic effects in a rat model of fibromyalgia. 3164 6


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