Nitrous Oxide Analgesia Research Articles

Regional lipid composition in the rat brain.

The lipid composition of the brain is of great importance to its metabolism and function. Although much research has been done on regional brain lipid composition, studies usually suffer from limited brain regions or from limited lipids analyzed. We modified a previously described method for the separation of brain phospholipids and glycolipids, improving the separation and sensitivity of the method. Using this modified method, we measured the lipid composition of the frontal and entorhinal cortices, the hippocampus, basal ganglia, cerebellum, and medulla oblongata of five rats under nitrous oxide analgesia. Total lipid content was highest (p < 0.05) in the medulla oblongata (111.0 +/- 6.0 mg/g wet brain, X +/- SD) followed by the hippocampus (72.6 +/- 2.8), cerebellum (62.7 +/- 4.6), basal ganglia (62.6 +/- 1.5), frontal cortex (57.7 +/- 2.1), and entorhinal cortex (53.3 +/- 1.9). The areas with higher total lipid content (p < 0.05) also had higher percentages of cerebrosides (18.6 +/- 2.2 in the medulla oblongata vs 8.3 +/- 1.2 in the frontal cortex) and 40 to 50% lower levels of phosphatidylcholine and phosphatidylinositol. The relation between the ratio of cerebrosides plus sulfatides to phosphatidylcholine and the total lipid content indicates that differences in brain lipid composition between regions are attributable to their relative gray/white matter content.

Clinical study of diffusion hypoxia after nitrous oxide analgesia : Quarnstrom FC, Milgrom P, Bishop MJ, et al. Anesth Prog 38:21, 1991

Clinical study of diffusion hypoxia after nitrous oxide analgesia : Quarnstrom FC, Milgrom P, Bishop MJ, et al. Anesth Prog 38:21, 1991

Sensory experience induced by nitrous oxide analgesia : Kaufman E, Galili D, Furer R, et al. Anesth Prog 37:282, 1990

Sensory experience induced by nitrous oxide analgesia : Kaufman E, Galili D, Furer R, et al. Anesth Prog 37:282, 1990

Placebo and Analgesic Nitrous Oxide for Treatment of the Alcohol Withdrawal State

We present evidence that analgesic (as distinct from anaesthetic) nitrous oxide is superior to placebo in the treatment of the alcohol withdrawal state. 'Carbogen' as a placebo is as effective as oxygen or medical air. However, placebo alone offers a means of treating the alcohol withdrawal state with a minimum of pharmacological intervention. Analgesic nitrous oxide for those not responding to placebo is a very rapid, effective, and extremely safe treatment which also reduces the use of highly addictive sedative pharmacological agents. This therapy also provides a rapid method of screening those patients requiring intensive monitoring and treatment in hospital from those who might benefit from out-patient therapy alone.

Analgesic nitrous oxide: rapid, safe therapy for addictive withdrawal

Analgesic nitrous oxide: rapid, safe therapy for addictive withdrawal

Opioid Effects of Analgesic (Subanesthetic) Nitrous Oxide on the Alcohol Withdrawal State

Annals of the New York Academy of SciencesVolume 625, Issue 1 p. 784-785 Opioid Effects of Analgesic (Subanesthetic) Nitrous Oxide on the Alcohol Withdrawal State MARK A. GILLMAN, MARK A. GILLMAN South African Brain Research Institute 6 Campbell Street Waverley 2090, Johannesburg, South AfricaSearch for more papers by this authorFREDERICK J. LICHTIGFELD, FREDERICK J. LICHTIGFELD South African Brain Research Institute 6 Campbell Street Waverley 2090, Johannesburg, South AfricaSearch for more papers by this author MARK A. GILLMAN, MARK A. GILLMAN South African Brain Research Institute 6 Campbell Street Waverley 2090, Johannesburg, South AfricaSearch for more papers by this authorFREDERICK J. LICHTIGFELD, FREDERICK J. LICHTIGFELD South African Brain Research Institute 6 Campbell Street Waverley 2090, Johannesburg, South AfricaSearch for more papers by this author First published: June 1991 https://doi.org/10.1111/j.1749-6632.1991.tb33919.xCitations: 5AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article.Citing Literature Volume625, Issue1Molecular and Cellular Mechanisms of Alcohol and AnestheticsJune 1991Pages 784-785 RelatedInformation

Combination therapy with carbamazepine/benzodiazepine for polydrug analgesic/depressant withdrawal

We describe the use of combination therapy with carbamazepine and benzodiazepine (BZ) for treating 4 cases of polydrug analgesic/depressant withdrawal. Carbamazepine appears to be effective in BZ withdrawal through its agonistic action on the peripheral benzodiazepine receptor. In cases where opioid abuse is suspected, analgesic nitrous oxide appears the most suitable agent to be added to this regimen, in view of its opioid properties, rapidity of action, and synergistic actions with benzodiazepines in ameliorating withdrawal from benzodiazepines and alcohol.

Analgesic nitrous oxide in alcohol withdrawal: The role of melatonin

Analgesic nitrous oxide in alcohol withdrawal: The role of melatonin

The drug management of severe alcohol withdrawal syndrome

We describe the various phases of the alcohol withdrawal syndrome with special reference to the pitfalls of using neuroleptics. We outline the importance of adequate sedation using either benzodiazepines or chlormethiazole. We provide a critical appraisal of the currently employed anti-epileptic medication in the alcohol withdrawal syndrome. We also indicate the usefulness of analgesic nitrous oxide as a screening test in differentiating the cases of alcohol withdrawal syndrome needing further intensive therapy to prevent progression to delirium tremens.

Influence of Chronic Ethanol Exposure on Nitrous Oxide Analgesia in Mice

The purpose of this study was to determine whether sensitivity to nitrous oxide analgesia was altered by chronic ethanol exposure. Control mice exposed to 25%, 50%, and 75% nitrous oxide in oxygen demonstrated a concentration-related analgesic effect, as measured by the acetic acid abdominal constriction test. Other mice previously exposed to ethanol vapors for 72 h exhibited a significantly reduced sensitivity to nitrous oxide analgesia. The dose-response curve of the chronic ethanol-exposed group was shifted to the right of that of the control mice. These findings suggest the possibility that subjects with a history of alcohol abuse might have reduced responsiveness to nitrous oxide in a clinical setting.

Analgesic nitrous oxide for alcohol withdrawal: a critical appraisal after 10 years' use

We describe a method of treating the mild to moderate alcohol withdrawal state which has been used successfully for 10 years in over 7,000 cases. It is now the standard therapy at the largest dedicated alcoholic rehabilitation centre in Southern Africa. The technique uses analgesic (subanaesthetic) concentrations of nitrous oxide, which in most cases is administered on a single occasion for 20 minutes only. This results in the most rapid detoxification presently available, such that within an hour of the commencement of therapy the patient is so improved that they can eat the next ward meal. Provided the correct equipment and simple training is used this non-anaesthetic treatment is completely free of any serious side effects and the patient is at all times conscious and cooperative. Apart from this the amounts of sedative medication, such as benzodiazepines, are drastically reduced during detoxification. Because of the rapidity of the therapeutic response this technique is useful also as a screening test for assessing those patients requiring intensive therapy for the alcohol withdrawal state. There is evidence of the usefulness of analgesic nitrous oxide therapy for treating other addictive withdrawal states including opioid and nicotine.

An evaluation of nitrous oxide analgesia during transcutaneous pacing.

Transcutaneous cardiac pacing (TCP) is a promising prehospital intervention, but there are little data available regarding protocols to improve patient tolerance to TCP. A 50:50 nitrous oxide:oxygen analgesic mixture also is a commonly employed prehospital intervention. In this randomized, prospective study, we compared the discomfort experienced by 18 healthy subjects when paced in two trials at the capture threshold: one following breathing of a 50:50 nitrous oxide:oxygen mixture; and the second only breathing room air. Discomfort was rated on an analog scale from 1 (minimal discomfort) to 10 (severe pain). Of the 18 subjects, 15 (83%) reported that nitrous oxide improved the tolerance to pacing at capture threshold. The median pain scores at capture threshold in the nitrous oxide and room air group were 3.8 and 5.0 respectively (P less than .05). Nine of the subjects tolerated TCP for the maximum allotted time of 30 seconds in each trial; six tolerated TCP for a longer time period in the nitrous oxide trial; three tolerated TCP longer in the room air trial. These data suggest that inhalation of 50:50 nitrous oxide:oxygen mixture may improve tolerance to TCP in the conscious patient.

Nitrous oxide analgesia in a pediatric emergency department : Gamis A, Knapp J, Glenske J. Ann Emerg Med. 1989;18:177–181

Nitrous oxide analgesia in a pediatric emergency department : Gamis A, Knapp J, Glenske J. Ann Emerg Med. 1989;18:177–181

Mediation of nitrous oxide analgesia in mice by spinal and supraspinal κ-opioid receptors

Exposure to nitrous oxide produced concentration-dependent analgesia in the mouse abdominal construction test. Intracerebroventricular or intrathecal pretreatment with naltrexone or nor-binaltorphimine significantly reduced nitrous oxide analgesia. However, similar pretreatment with β-funaltrexamine had no appreciable effect. These findings suggest that nitrous oxide analgesia involves spinal and supraspinal κ-opioid receptors.

Analgesic nitrous oxide as an investigative and therapeutic agent in psychiatry

Analgesic nitrous oxide as an investigative and therapeutic agent in psychiatry

Nitrous oxide analgesia in a pediatric emergency department

Nitrous oxide (N2O) has been shown to be an effective analgesic in adult medical outpatients, yet no prospective studies of its use in the pediatric medical outpatient exist. Thirty-four children requiring laceration repair were randomly assigned to one of two treatment groups: 30% N2O/70% O2 or a placebo, 100% O2. Pain behavior, using the observer-scored Children's Hospital of Eastern Ontario Pain Scale, was assessed by double-blind techniques, before and during the laceration repair. Less pain behavior was seen in children less than 8 years old who received the N2O mixture than in those receiving the placebo. In patients 8 or more years old who received N2O, there was a significant improvement in the second evaluation as compared with those receiving only O2 during the procedure (P less than .05). There also was a smaller increase in pain behavior, from the first to the second evaluation, in those receiving N2O (P less than .05). No side effects were encountered. The authors conclude that continuous N2O inhalation is an effective and painless analgesic in children for outpatient procedures. More effective analgesia will likely occur with 40% to 50% N2O, although these concentrations remain to be studied in pediatric outpatients.

Stereospecific reversal of nitrous oxide analgesia by naloxone

The opiate antagonist naloxone was found to block nitrous oxide analgesia in a stereospecific fashion. Using a modified hotplate test in mice, the (−)-enantiomer of naloxone (which has a K D of ≈ 1 nM for opiate receptors) antagonized the analgesic actions of nitrous oxide in a dose-dependent (2.5–20 mg/kg) fashion. In contrast, the (+)-enantiomer (K D ≈ 10,000 nM) had no effect on nitrous oxide analgesia at the highest dose tested (40 mg/kg). These data strongly suggest that nitrous oxide analgesia is mediated via opiate receptors and is consistent with the hypotheses that this effect occurs either through the release of endogenous opioids or by physical perturbation of the opiate receptors.

Antistress Hormonal Responses of Analgesic Nitrous Oxide

We briefly describe the hormonal responses associated with stress and provide evidence that endogenous and exogenous opioids have "antistress" hormonal profiles. We present data which indicate that analgesic nitrous oxide produces a typical opioid hormonal response, viz. increased prolactin and decreased cortisol levels. There was no significant change in ACTH levels despite the fall in cortisol. We present evidence which supports the hypothesis that the antistress hormonal effects of opioids and analgesic nitrous oxide are mediated by uncoupling the adrenal gland from hypothalamico-pituitary stimulation. It would appear that the opioid system acts antagonistically to the adrenocortical system in stress. We propose that any method stimulating the opioid system optimally may have the antistress effects.

Analgesic nitrous oxide in neuropsychiatry: past, present and future.

We highlight the distinction between analgesic and anesthetic concentrations of nitrous oxide, with special reference to the safety of analgesic nitrous oxide. We present evidence that the gas at analgesic concentrations is an opioid agonist. Its extremely low abuse potential, despite its opioid properties, is discussed with regard to its evanescent action and possible partial agonistic effects, making it the least addictive of all mind-altering addictive substances. The activities of analgesic nitrous oxide make it an almost ideal agent with which to investigate the functions of the opioid system in man. We also discuss its use as a diagnostic and therapeutic agent in neuropsychiatry.

A measurement of cerebral glucose uptake rate by 31P MRS

A method for the measurement of cerebral glucose uptake rate by in vivo 31P Magnetic Resonance Spectroscopy (MRS) is proposed. The initial rate of 2-deoxy-glucose (DG) uptake after DG administration is measured by the increase of 2-deoxy-glucose-6-phosphate (DG6P) signal at a chemical shift of 7.2 ppm with respect to phosphocreatine (PCr). The values for four different metabolic states of rat brain (two levels of epileptic seizures induced by bicuculline, nitrous oxide analgesia and pentobarbital anesthesia) were in good agreement with the previously reported ones by radioisotope methods. This method appears to be useful for measuring cerebral glucose uptake rate.