Nitrous Oxide Analgesia Research Articles

Cognitive Reversal of Expected Nitrous Oxide Analgesia for Acute Pain

In a laboratory experiment, the expected analgesic action of 33% nitrous oxide was reversed by creating the expectancy of heightened awareness of bodily sensations. Pain threshold and tolerance of electrical tooth-pulp stimulation were significantly reduced. Results from a control study gave us a basis for comparison of changes in the verbal expression of pain when nitrous oxide was administered without introducing expectancies beyond those already held by the subjects. Contrasting results from the experimental and control studies confirm the powerful role of mental processes in mediating pain experience.

Postoperative Nitrous Oxide Analgesia and the Functional Residual Capacity

Postoperative Nitrous Oxide Analgesia and the Functional Residual Capacity

Entonox for casualties at 1000 m: use of nitrous oxide analgesia in Nigeria at moderate altihnle

Entonox for casualties at 1000 m: use of nitrous oxide analgesia in Nigeria at moderate altihnle

Nitrous Oxide Analgesia for Refractory Pain in the Terminally III

Nitrous oxide analgesia was used in the management of the terminal hospitalization of four adolescents and one child with disseminated cancer. All patients had severe pain that was unresponsive to standard regimens of narcotics and various narcotic analgesia-stimulant combinations. In each case, the addition of nitrous oxide led to an obvious improvement in symptoms of pain, anxiety, and agitation, while simultaneously improving appetite, mood, and the capacity to communicate. There were no side effects except those related to the discomfort of wearing a mask. Acceptance of the procedure by patient, family, and staff was universal and enthusiastic. The procedure is safe, easily administered, and noninvasive. Nitrous oxide can be useful in managing terminal illness refractory to standard pain control measures.

Nitrous oxide analgesia for refractory pain in the terminally ill

Nitrous oxide analgesia for refractory pain in the terminally ill

Cerebral metabolic studies in vivo by 31P NMR.

31P NMR studies on the brains of living rabbits were carried out at 32 MHz in a spectrometer having a 200-mm clear bore. Paralyzed pump-ventilated animals under nitrous oxide analgesia were inserted into the 1.89-T field and signals were focused in the brain by using a 4-cm surface coil. Several conventional physiological variables were monitored together with 31P spectra during induction and reversal of insulin shock and hypoxic hypoxia sufficient to abolish the electroencephalogram and during status epilepticus. A reversible decrease in phosphocreatine stores accompanied by an increase in Pi was detected during hypoglycemia and hypoxia. Similar changes were observed in prolonged status epilepticus but were not reversed. ATP levels fell about 50% in hypoglycemia but only slightly in the other two metabolic stresses. Intracellular pH rose in hypoglycemia; in status epilepticus and hypoxia it fell, but only when cardiovascular function was severely impaired. From the measured NMR parameters and the assumptions (i) that creatine kinase was at equilibrium and (ii) that the creatine/phosphocreatine pool was constant, it was possible to calculate the relative changes in cytoplasmic ADP levels associated with these metabolic disturbances.

Postoperative nitrous oxide analgesia and the functional residual capacity

Surgery of the upper abdomen is associated with the greatest demand for postoperative analgesia and also is marked by depressed pulmonary function, arterial hypoxemia, and pulmonary complications. Nitrous oxide (N2O) in concentrations of 15-25% is a potent analgesic and is relatively free of untoward side effects if administered for a maximum of 48 h. In the present study, the effect of N2O analgesia on postoperative lung function, in particular, the functional residual capacity (FRC), is examined. Eighteen cholecystectomy patients received either a narcotic (N = 11) or N2O (N = 7) for postoperative analgesia. N2O-treated patients had satisfactory analgesia and maintained FRC at normal levels. Narcotic treated patients had a fall of 22% in FRC. N2O had no effect on the formed elements in peripheral blood.

The effects of nitrous oxide and naloxone on orgasm in human females: A preliminary report

Abstract The effect of nitrous oxide and naloxone, alone and in combination, on female orgasm was investigated. Nitrous oxide enhanced sexual fantasy, whereas naloxone dose—dependency given immediately prior to orgasm—either heightened or diminished sexual pleasure. The bimodal pattern suggests the possibility that the same dual biological system which mediates pain perception may also mediate orgasm. The possible use of nitrous oxide analgesia, with or without naloxone, as a diagnostic, experimental, and therapeutic tool is discussed.

Naloxone fails to antagonize nitrous oxide analgesia for clinical pain.

Abstract In 30 patients with dental postoperative pain we tested the hypothesis that the analgesic effects of nitrous oxide (N2O), a mild analgesic, may be mediated via endogenous opioids. Using the visual analog scale to assess pain, significant analgesia was induced by 33% N2O. N2O-induced analgesia was not significantly antagonized by 10 mg of intravenous naloxone. In the setting of clinical pain there appears to be little if any contribution of endogenous opioids to N2O-induced analgesia.

Assembly of an inexpensive tail flick analgesia meter

The construction of an inexpensive (⋍$100) digital tail flick analgesia meter is described. The design incorporates a projection lamp as the radiant heat source and automatic timing of the tail flick. Its use in assessing nitrous oxide analgesia in rats is described.

Antagonism of Nitrous Oxide Analgesia by Naloxone in Man

Antagonism of Nitrous Oxide Analgesia by Naloxone in Man

Fast Oscillatory EEG Activity Induced by Analgesic Concentrations of Nitrous Oxide in Man

EEGs during inhalation of analgesic concentrations of 30%, 50%, and 70% nitrous oxide in oxygen, in the absence of other medication were studied in man. Although nitrous oxide has been considered to produce no significant change in EEG activity, it was found to produce characteristic fast oscillatory activity (FOA) in a predictable fashion. FOA was associated with unconsciousness or unresponsiveness to stimuli and appeared predominantly in the frontal areas. Power spectrum analyses showed that the frequency of FOA was remarkably constant across subjects and across trials with a peak frequency of 34 Hz. Amplitude and quantity of FOA increased as the concentration of nitrous oxide increased approaching 100 microV and more than 90%, respectively, under 70% nitrous oxide. It took approximately 1 hour after cessation of nitrous oxide before EEGs had completely returned control pattern with little FOA in spite of expected rapid decrease of alveolar nitrous oxide concentration. FOA can serve as a clinical monitor of the effectiveness of nitrous oxide analgesia.

Effects of indomethacin on cerebral blood flow and oxygen consumption in barbiturate-anesthetized Normocapnic and hypercapnic rats.

Although results obtained in baboons and rats have demonstrated that the fatty acid cyclo-oxygenase inhibitor indomethacin reduces cerebral blood flow (CBF) under control conditions and markedly attenuates the CBF response to hypercapnia, nonconfirmatory results have been obtained in rabbits and cats. Since these latter studies were carried out under barbiturate anesthesia, we tested the effect of indomethacin (10 mg kg-1) on CBF and cerebral oxygen consumption in rats anesthetized with 150 mg kg-1 of phenobarbital. At normocapnia the barbiturate reduced CBF, measured with a 133Xe modification of the Kety-Schmidt technique, to about 50% of nitrous oxide control values as previously determined with a similar technique. At this CBF level, indomethacin induced a small, albeit highly significant decrease in CBF. We suggest that a reduction of this magnitude will escape detection with some CBF techniques in current use. Indomethacin induced a highly significant decrease in CBF during hypercapnia, demonstrating that the barbiturate does not eliminate the effect of indomethacin on CO2 responsiveness. The magnitude of the reduction in CO2 response was so large that is should be detected with most methods for measuring CBF. A comparison with previous data on animals under 70% N2O demonstrated that phenobarbital reduced the CO2 responsiveness. defined as the ratio deltaCBF/deltaPCO2, to 39% of that observed under nitrous oxide analgesia. With both types of anesthesia, indomethacin curtailed the CO2 responsiveness 4- to 5-fold.

A comparison of the effects of morphine sulphate and nitrous oxide analgesia on chronic pain states in man

The effect of nitrous oxide and morphine sulphate on chronic pain states in man are compared. The similarity of effect indicate that nitrous oxide acts on the morphine receptor. In all cases where analgesia was produced naloxone reversal occurred. These results provide additional evidence for a dual system hypothesis of pain perception and that nitrous oxide analgesia is mediated by the endogenous opiate system. In the light of these findings, the possibility of using nitrous oxide to replace morphine sulphate as a screening test for deep brain stimulation analgesia is discussed.

Nitrous-oxide analgesia during ambulance transportation. Airborne levels of nitrous oxide.

A model experiment was performed for studying nitrous-oxide levels in the breathing zones of the different members of an ambulance team, viz. the anesthetist, the accompanying person in the ambulance coupé, and the ambulance driver. Without a functioning local exhaust coupled to the exhalation valve, the integrated average level of nitrous oxide in the breathing zone of the anesthetist was 650-1,700 ppm, with top concentrations up to 7,500 ppm. Under the same conditions, the accompanying person in the ambulance coupé was exposed to average concentrations of 58-280 ppm, with top concentrations up to 660 ppm. The mean exposure of the driver was 9-45 ppm (max. 81 ppm). However, the exposure to nitrous oxide was considerably decreased in all parts of the ambulance by an effective local exhaust system. A prerequisite for nitrous-oxide analgesia in ambulances is an effective local exhaust coupled to the exhalation valve or face mask. The ambulance coupé ought to be equipped with a motor-driven exhaust fan in the roof, the ordinary inlet fan of the ambulance should be switched on at maximum speed, and any additional heater or fan in the ambulance coupé should be placed inside the coupé and not behind the driver's seat.

Recovery and Enhancement of Reflex Reaction Time after Nitrous Oxide Analgesia

The findings of this study substantiate the assumption that psychomotor impairment is rapidly reversed following the administration of nitrous oxide. The concern of clinicians is to determine the optimum oxygenation period after administration of N2O and to show whether there is a need for prolonged observation before the patient can be released. Generally, under short-term conditions such as are used in conjunction with outpatient dental treatment, the patient should be largely recovered after a five-minute exposure to 100% oxygen at the conclusion of the appointment. However, further benefit apparently is gained from a somewhat longer time of recuperation before engaging in any activity requiring extracting psychomotor skills. The results of this study indicate that 15 minutes is an appropriate delay after relatively short exposure to N2O. It cannot be determined from this study whether longer-term exposure, such as the periods involved in complicated restorative procedures, would require longer recovery periods for certain individuals.

The closed co-axial analgesia system.

A twin-tube system for nitrous oxide analgesia in dental surgeries is described. The system is a non-polluting modification of the Mapleson A system, employing the principle of co-axial tubing introduced by Bain & Spoerel (1972). Active, continuous and calibrated gas removal takes place via the co-axial tubing by means of an ejector flowmeter. Investigation of the dynamic pressure excursions occurring at the nose-piece are fully compatible with normal breathing. Gas contamination of the dental environment can be reduced by at least 90%. The system described is safe and easy to handle. It is made of light-weight material and is adaptable to the equipment available. No rebreathing takes place when using a fresh gas inflow of 150 ml/kg body weight/min.

Self-Administered Intermittent Nitrous Oxide Analgesia for Labour. Enhancement of Effect with Continuous Nasal Inhalation of 50 Per Cent Nitrous Oxide (Entonox)

Departments of Anaesthesia, Maelor General Hospital and University Hospital of Wales, Cardiff, Wales

Paradoxical effect of naloxone on nitrous oxide analgesia in man

The effect of naloxone on nitrous oxide analgesia in man has been investigated. The paradoxical response so obtained indicates the possibility of a dual system mediating the pain response in man. These results support previous animal experiments indicating that nitrous oxide analgesia is mediated by the opiate receptors.

Tolerance to nitrous oxide analgesia in rats and mice.

The purpose of these experiments was to characterize the nature of tolerance to the analgesic action of nitrous oxide. Analgesia was assessed in rats using a tail-flick latency test and in mice using an abdominal constriction test. Rats and mice were exposed to nitrous oxide, 75 per cent, the balance oxygen, continuously for 16--18 hours. On re-exposure to nitrous oxide 30 min later, these animals were found tolerant to nitrous oxide in that the analgesic response was decreased by at least 50 per cent. Animals tolerant to nitrous oxide were not tolerant to morphine. Morphine (0.25--1.5 mg/kg) produced equal degrees of analgesia in control and nitrous oxide-tolerant mice and rats. In contrast, rats made tolerant to morphine by repeated daily injections of as much as 400 mg/kg subcutaneously or by subcutaneous implantation of morphine pellets (75 mg, twice) showed a decreased analgesic response to nitrous oxide. Thus the cross-tolerance between nitrous oxide and morphine appears unique in that it is unidirectional.