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

In experiments on white rats the generator of excitation was created in the dorsal raphe nucleus by microinjection of tetanus toxin. After formation of the excitation generator electrical activity in this nucleus was changed as the following: the first negative component (N1) was strongly increased, general EP configuration changed and the spontaneous paroxysmal activity became more frequent. The time of the generator formation correlated with the appearance of intense and prolonged analgesia. Naloxone did not reverse the effects of analgesia described.
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PMID:[Analysis of analgesia induced by the generator of excitation in the dorsal raphe nucleus]. 51 16

A systemically active enkephalin analogue, FK33824, given intravenously depressed dorsal root potentials in cat spinal cord. The negative DR V and positive DR VI, measured by computer, were both decreased; this effect was reversed by small doses of intravenous naloxone. Naloxone, given alone, with no previous analogue produced no changes in dorsal root potentials suggesting the absence of a basal enkephalin tone. A second injection of FK33824 was much less effective that the first dose. The results were discussed in relation to presynaptic mechanisms for analgesia: we proposed that FK33824 causes presynaptic inhibition by modulation rather than by depolarization of primary afferent fibers.
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PMID:Effects of enkephalin analogue and naloxone on cat spinal cord dorsal root potentials. 52 66

Naloxone (5 mg/kg subcutaneously) failed to effect significantly the reaction of electric self-stimulation in rats with electrodes implanted into lateral hypothalamic area. In 3 rats the analgesic effect manifested in an increase of the threshold of painful vocalization under electrostimulation of the tail was revealed. The antinociceptive effect was abolished with naloxone. Morphine (3 mg/kg) potentiated self-stimulation while naloxone antagonized this action. The role of opiate receptors in effects of self-stimulation and centrally produced analgesia is discussed.
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PMID:[Action of naloxone on emotionally positive and antinociceptive effects of hypothalamic stimulation in rats]. 54 Jan 48

The analgesic properties of lidocaine and morphine were compared in mice using a hot plate stimulus. An analgesic response was defined as an increase in the time required for an animal to attempt to escape by jumping. When compared to saline-treated controls, lidocaine produced a statistically significant dose-related delay in response to heat. Dose-response curves for morphine and lidocaine indicated that morphine has greater potency and efficacy. Naloxone (1.0 mg/kg) reversed the analgesic response due to morphine (10 mg/kg) but had no effect on the analgesia produced by lidocaine (50 mg/kg).
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PMID:Analgesic properties of lidocaine in mice. 57 Dec 51

Animals exposed to cold-water swims, rotation, or inexcapable shocks, display analgesia comparable to that of 10 mg/kg of morphine. The present study investigated whether a narcotic antagonist would eliminate analgesia induced by cold-water swims. In one group of 12 rats, naloxone at 0, 1, 5, 10 and 20 mg/kg was administered at weekly intervals immediately preceding forced cold-water swims (2 degrees C for 3.5 min) and alterations in flinch-jump thresholds were determined 30 min thereafter. In a second group of six rats, the effects of the same dose range of naloxone were determined upon normal flinch-jump thresholds. Naloxone dose-dependently attenuated the cold-water swim-induced analgesia up to a maximal reduction of 50% at 20 mg/kg. In contrast, all doses of naloxone had no effects upon normal flinch-jump thresholds. Since low doses of naloxone completely abolish morphine-induced analgesia, the present data suggest that the analgesia induced by stress is not identical to that of opiates.
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PMID:Dose-dependent reductions by naloxone of analgesia induced by cold-water stress. 69 50

A biphasic dose-response pattern is generated by the isoquinoline, 3-carboxysalsolinol, in analgesia tests conducted in mice. Carbidopa pretreatment enhances this effect, as well as the morphine-induced analgesic increase by 3-carboxysalsolinol. Naloxone blockade of all of these responses suggests an interaction of the alcohol-based isoquinoline with central opiate receptors.
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PMID:Analgesic effects of 3-carboxysalsolinol alone and in combination with morphine. 89 38

Potent analgesia results from electrical stimulation of the periaqueductal grey matter in several species including man. Electrophysiological experiments indicate that this electrical analgesia could result from the activation of descending influences which inhibit the activity of dorsal horn interneurons in the transmission of painful messages. Numerous physiological, behavioral and pharmacological studies mention that the descending serotoninergic Bulbo-spinal system plays a major role in electrical analgesia. Several studies suggest that both electrical and morphine analgesia share, at least in part, a common site and mechanism of action. This possibility is mainly supported by the fact that analgesia induced by electrical stimulation is suppressed or reduced by a specific opiate antagonist (Naloxone).
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PMID:[Analgesia: role of the brainstem (author's transl)]. 90 15

Peripheral electrical stimulation of the rat produced a "dose-dependent" analgesia both in intact and in spinal animals. Naloxone, a narcotic antagonist, almost completely reversed this analgesia. It is felt that peripheral electroanalgesia acts via the release of endogenous narcotic-like substances, the enkephalins, at spinal and supraspinal centres.
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PMID:Naloxone-reversible peripheral electroanalgesia in intact and spinal rats. 92 40

The objective of this study was to characterize further the nature of nitrous oxide analgesia and to establish if tolerance to nitrous oxide occurs. Methods for studying the analgesic action of a gas are described. In mice, nitrous oxide is analgesic in the phenylquinone and acetic acid abdominal constriction tests. Aspirin and very high doses of alcohol are also active in these tests; however, only nitrous oxide-induced analgesia is antagonized by narcotic antagonists. These data indicate the mechanism of action of nitrous oxide analgesia differs from that of the other two drugs. Nitrous oxide produced a dose-related analgesic response in rats (ED50, 67%) as measured by the tail-flick method. Naloxone, 5 to 30 mg/kg, also antagonized nitrous oxide analgesia in rats. Lower doses of the antagonist were not effective. Tolerance developed to the effects of nitrous oxide in both rats and mice after prolonged exposure. These data lend support to the hypothesis that nitrous oxide and opiates have a significant pharmacologic resemblance and may ultimately produce similar molecular events in the brain leading to the relief of pain.
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PMID:Nitrous oxide analgesia: reversal by naloxone and development of tolerance. 92 57

In this comparative study, the abdominal constriction test was used to determine analgesia in mice, and the body plethysmograph was used to study respiratory effects of nalodeine, nalorphine, naloxone, codeine, morphine and various agonist-antagonist combinations in rats. The analgesia dose-response curves for the surrogate pairs, nalodeine-nalorphine and codeine-morphine, were parallel but had significantly different slopes. Naloxone was a more potent antagonist of morphine and codeine than of nalorphine and nalodeine. In antagonizing morphine and codeine analgesia, naloxone was the most potent antagonist, nalorphine had a biphasic effect with decreasing activity at higher doses and nalodeine was not an antagonist. Moderate doses of nalorphrine depressed minute volume largely by their effect on tidal volume, but high doses stimulated respiratory rate and therefore had less effect on minute volume. Nalodeine depressed minute volume by depressing tidal volume, since all doses initially stimulated and then variably affected respiratory rate. Metabolic rate was not increased by either drug short of convulsant doses. Nalodeine depresses the ventilatory response to CO2 and weakly antagonizes the respiratory depressant actions of morphine.
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PMID:A comparative study of the analgesic and respiratory effects of N-allylnorcodeine (nalodeine), nalorphine, codeine and morphine. 94 29


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