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

The object of this study was the use of naloxone to correct hypoventilation related to the use of morphinomimetics without suppressing the analgesic effect of these agents. The study involved ten patients undergoing gynaecological surgery under neuroleptanalgesia and who at the end of surgery had hypoventilation due to the use of fentanyl (average dose : 4.87 microgram/kg/h) or phenoperidine (average dose : 48.7 microgram/kg/h). Naloxone was administered intravenously in an average dose of 1.37 microgram/kg (in one or two injections) followed by an intramuscular injection of an average of 0.73 microgram/kg. Under these conditions, respiratory depression was completely corrected in all cases, the effect being durable. Good analgesia was retained and there was a normal return to consciousness without undesirable effects.
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PMID:[Antagonistic effects of naloxone against morphinomimetic agents. Apropos of 10 cases in gynecologic surgery]. 2 37

The effect of naloxone on dental postoperative pain was studied to examine the hypothesis that endorphins mediate placebo analgesia. All patients had extraction of impacted mandibular third molars with diazepam, N2O, and local block with mepivacaine. 3 h and 4 h after surgery naloxone or a placebo was given under randomised, double-blind conditions. Pain was evaluated on a visual analogue scale. Patients given naloxone reported significantly greater pain than those given placebo. Patients given placebo as their first drug was either placebo responders, whose pain was reduced or unchanged, or nonresponders whose pain increased. Naloxone given as a second drug produced no additional increase in pain levels in nonresponders but did increase pain levels of placebo responders. Nonresponders had a final mean pain rating identical to that of responders who received naloxone as their second drug. Thus the enhancement of reported pain produced by naloxone can be entirely accounted for by its effect on placebo responders. These data are consistent with the hypothesis that endorphin release mediates placebo analgesia for dental postoperative pain.
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PMID:The mechanism of placebo analgesia. 8 May 79

Rats treated with Lilly 110140, a specific inhibitor of serotonin re-uptake in brain, are less sensitive to electroshock. Lilly 110140 antagonizes the hyperalgesia following injections of p-chlorophenylalanine and potentiates morphine analgesia. Naloxone blocks the analgesia following morphine, but has no effect on Lilly 110140-induced analgesia. Brain serotonin neurons may, at least in part, mediate analgesia.
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PMID:Analgesic effect of fluoxetine hydrochloride (Lilly 110140), a specific inhibitor of serotonin uptake. 13 83

Narcotic analgesics and related drugs act as agonists on several receptors that are responsible for their effects on pain perception, mood and feeling state, and respiration, as well as other pharmacologic actions. Naloxone is the first discovered antagonist that is devoid of agonistic activity and appears to be a competitive antagonist at several receptors. The ability of naloxone to displace or prevent the binding of agonistic narcotics is partly responsible for its antagonistic effects. The ability of naloxone to rectify narcotic-depressed homeostats and precipitate abstinence is also related to its antagonistic activity. Certain cautions and principles apply in the use of naloxone in treating narcotic overdose, reversing surgical analgesia, and the treatment of neonates and children. Unapproved uses of naloxine include reversing the psychotomimetic effects of certain agonists-antagonists, terminating narcotic-induced convulsions and coma, reversing non-narcotic depression, diagnosing physical dependence, and treating narcotic addicts.
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PMID:Naloxone. 18 95

1 In spinal cats anaesthetized with alpha-chloralose, a study was made of the effects of morphine and naloxone, administered electrophoretically from micropipettes, on the responses of dorsal horn neurones to noxious (raising of skin temperature above 45 degrees C) and innocuous (deflection of hairs) peripheral stimuli.2 Administered near cell bodies, morphine reduced the nociceptive responses of only 2 of 37 cells. Excitation occurred more commonly than depression and abnormalities in action potentials were commonly observed following ejection of morphine. None of these effects of morphine was antagonized by electrophoretically applied naloxone.3 Administered in the substantia gelatinosa from one micropipette while recording responses of deeper neurones with a second micropipette, morphine reduced the nociceptive responses of 15 of 19 neurones. Firing in response to deflection of hairs was not reduced by morphine. Depression of nociceptive responses by morphine was long lasting (>20 minutes). Naloxone ejected into the substantia gelatinosa or given intravenously in doses as low as 0.1 mg/kg antagonized the effects of morphine. The effectiveness of this dose of intravenous naloxone suggests that the concentrations of morphine in the substantia gelatinosa which reduced nociceptive responses were not unlike those present after analgesic doses of systemic morphine. Naloxone alone, and excitant and depressant amino acids ejected into the substantia gelatinosa had little effect on cell firing.4 Both the selective action of morphine on nociceptive responses and the reversal of this action by intravenous naloxone suggest that the opiate receptor present in the substantia gelatinosa is relevant to analgesia produced by opiates given systemically.
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PMID:Suppression of transmission of nociceptive impulses by morphine: selective effects of morphine administered in the region of the substantia gelatinosa. 19 11

In a dose-response study, 7.5 mg/kg of naloxone produced maximal attenuation of conditioned taste aversion to saccharin induced by 10 mg/kg of morphine. Naloxone was administered immediately after the morphine in this study. In a second experiment, naloxone still caused a significant attenuation of taste aversions when administered with a 1 hr delay after morphine, but not after delays of 4 or 8 hr. These results suggest that behavioral consequences of morphine which peak during the first hr after injection (analgesia, catalepsy, and depression of intracranial self-stimulation) are not correlated with the aversive effect of morphine. Nor can the aversiveness of morphine be attributed to withdrawal effects. Only the facilitative actions of morphine occurring 1 to 4 hr after injection, including the facilitation of intracranial self-stimulation, are temporally correlated with the naloxone-sensitive aversive effect. Thus, a temporal analysis cannot be used to dissociate the paradoxical positive reinforcement and aversive effects of morphine. Rather, the temporal correlation between the two opposite motivational effects of morphine serves to emphasize the nature of this paradox.
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PMID:Temporal analysis of naloxone attenuation of morphine-induced taste aversion. 26 68

Intraventricular administration of a peptide from ovine pituitaries whose structure is identical to the 61-91 C-terminal portion of beta-lipotropic hormone (61-91 beta-LPH) induced catalepsy, muscular hypertonus and analgesia in rats. Naloxone inhibited both the analgesic and cataleptic effects. 1-dihydroxyphenylalanine (1-DOPA) completely prevented the cataleptic effect. The cataleptic effect of 61-91 beta-LPH was potentiated by 1-5-hydroxytryptophan (5-HTP).
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PMID:Cataleptic effect of 61-91 beta-lipotropic hormone in rat. 30 38

Our paper is concerned with considerations of pain physiology in pyrovasy and with neuropharmacological effects of the Opiate antagonist Naloxone. These considerations explain the relationship of analgesia and hypersthesia with stress induced behavior and states of consciousness. Apart from psychophysiological aspects we can distinguish from a biochemical and neurophysiological point of view two mechanisms of pain perception in pyrovates: 1. Certain mechanical stimuli brought about by the individual running technique of the pyrovate cause convergence of noxis and non-noxic afferent impulses as well as central inhibition of the effect of noxic stimuli. 2. The long stressful period of preparations induces a temporary surplus of Endorphins elevating the pain threshold.
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PMID:[Psychophysiology of fire walking. II. Pain perception in pyrovasy (fire walking)]. 49 16

Acute administration of 2-deoxy-D-glucose (2-DG), an antimetabolic glucose analogue induces a powerful analgesia which adapts following repeated administration. 2-DG analgesia displays significant cross-tolerance with morphine, and like morphine analgesia, is potentiated in hypophysectomized rats. The present study examined further the role of opiates in 2-DG analgesia by examining whether the opiate antagonist, naloxone, would affect 2-DG analgesia, and whether ineffective doses of 2-DG and morphine would interact in a synergistic fashion to induce analgesia. Nociceptive thresholds were measured by the flinch-jump test. Naloxone doses of 1, 5, 10 and 20 mg/kg were all ineffective in reducing significantly 2-DG (600 mg/kg) induced pain threshold elevations. Naloxone failed to attenuate 2-DG (350 mg/kg) analgesia whether administered before or after the 2-DG injection. On the other hand, simultaneous administration of sub-analgesic doses of 2-DG (200 mg/kg) and morphine (2.5 mg/kg) summated to produce significant analgesia. This, 2-DG analgesia is similar to opiates in its tolerant and summative actions, yet dissimilar in that naloxone is ineffective in reversing its effects.
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PMID:2-Deoxy-D-glucose analgesia: influences of opiate and non-opiate factors. 50 9

A method is described for testing analgesia for narcotic or nonnarcotic drugs in rats injected with Freund's adjuvant in the tail, by manipulation of the tail the day after injection, or of the feet after the development of adjuvant arthritis. The method is responsive to a behavioral depressant or an anti-inflammatory steroid. Diflunisal (MK-647; 5-(2,4-difluorophenyl)salicylic acid] exhibited activity in this assay after oral administration with potency about 25 times greater than that of aspirin, about 3 times that of glafenine and twice that of zomepirac. The onset of activity was within a 1/2 hour for narcotic analgesics but required about an hour for non-narcotic compounds. With the latter, the peak of activity was not attained until 2 to 4 hr, depending on the compound. The peak for diflunisal was delayed until the 3rd or 4th hour, but the onset of action was more prompt and the duration greater as the dose was increased. [14C]Diflunisal was concentrated to some extent in the inflamed tissue after adjuvant injection. Peak levels both in plasma and tissue appeared about 2 hr before peak analgesic effect. Repeated administration of large doses produced neither tolerance nor sensitization to the analgesic action of diflunisal. Naloxone and naltrexone did not antagonize the action of the compound, but when morphine and diflunisal were given together, the overall effect was enhanced.
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PMID:Analgesic activity of diflunisal [MK-647; 5-(2,4-difluorophenyl)salicylic acid] in rats with hyperalgesia induced by Freund's adjuvant. 51 31


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