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

The analgesic effect of a 3-min swim stress was assessed using the formalin test. Male Swiss mice were injected i.p. with naloxone (0.1 or 1.0 mg/kg), MK-801 (0.075 mg/kg) or saline 15 min prior to swimming in water maintained at 20 degrees C or 32 degrees C. The mice were then injected with 20 microliters of 5% formalin into the plantar surface of 1 hind paw and pain behaviour (time spent licking the injected paw) was continuously monitored during the subsequent 10 min. Swim stress produced a significant reduction in pain behaviour at both 20 degrees C and 32 degrees C. MK-801 completely blocked the analgesia produced by both the 20 degrees C and 32 degrees C swim. At a dose of 0.1 mg/kg, naloxone partially antagonized the analgesia produced by the 32 degrees C swim but did not affect the analgesia produced by the 20 degrees C swim. Naloxone at a dose of 1.0 mg/kg had no effect on swim stress-induced analgesia. Neither MK-801 nor 0.1 mg/kg naloxone altered baseline pain behaviour, although 1.0 mg/kg naloxone did significantly reduce it. It is unlikely that the effect of MK-801 on swim stress-induced analgesia is due to an interaction with an opioid mechanism, as MK-801 had no effect on morphine analgesia. These results suggest that the analgesia produced by the 20 degrees C swim stress in the formalin test is non-opioid in nature and mediated via the NMDA receptor, whereas the 32 degrees C swim stress-induced analgesia has both an opioid and non-opioid component.
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PMID:NMDA receptor antagonist MK-801 blocks non-opioid stress-induced analgesia in the formalin test. 138 68

Naloxone (200 micrograms/kg, i.v.) reduced the noxious thermal stimuli-evoked responses of 16/25 nociceptive neurons in the superficial laminae whereas it enhanced the responses of 6/10 nociceptive neurons in the deeper dorsal horn. However, a different picture emerged when selectivity of neuronal responsivity (nocireceptive or multireceptive) was considered. In the superficial dorsal horn, naloxone reduced the responses of the majority of (15/18) selectively nocireceptive neurons. The reduction in responses became apparent within 60 sec following naloxone administration and returned to control level within 48 min. In contrast, the responses of the majority of multireceptive neurons in the superficial (6/7), or the deeper (6/10) dorsal horn, were enhanced. The excitatory action in the superficial dorsal horn persisted for only 6-15 min, whereas it persisted for 40-70 min in the deeper dorsal horn. The firing of the majority of cold-receptive neurons (6/8) in the superficial dorsal horn was not altered. These effects were stereoselective since (+)-naloxone, the inactive isomer of naloxone, did not affect the responses of 14/16 nociceptive neurons. It is concluded that naloxone differentially, and selectively, affects the firing of nociceptive neurons in the superficial versus the deeper dorsal horn, and the firing of selectively nocireceptive versus multireceptive neurons. The relevance of these findings to the behavioral effects of naloxone, hyperalgesia and analgesia, is discussed.
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PMID:Differential influence of naloxone on the responses of nociceptive neurons in the superficial versus the deeper dorsal horn of the medulla in the rat. 140 6

The effects of naloxone on the analgesic response were examined using the tail-flick test, in mice with streptozotocin-induced diabetes. Subcutaneous injection of naloxone (5 mg/kg, s.c.) produced a marked analgesia in diabetic mice but not in age-matched non-diabetic mice. Naloxone-induced analgesia in diabetic mice was significantly reduced by pretreatment with naltrindole (0.1 mg/kg, s.c.), a selective antagonist of delta-opioid receptors. By contrast, no significant naloxone-induced increase in tail-flick latency in diabetic mice was observed after chronic treatment with naloxone (5 mg/kg, s.c.) for 5 days. However, the tail-flick latency was significantly increased by chronic treatment with naloxone in non-diabetic mice. Furthermore, the significant naloxone-induced increase in tail-flick latency in non-diabetic mice that had been chronically treated with naloxone was also antagonized by pretreatment with naltrindole. Chronic pretreatment with 5 mg/kg of naloxone for 5 days markedly attenuated the analgesic effect of the delta-agonist DPDPE in diabetic mice, whereas this pretreatment significantly enhanced the effect of DPDPE in non-diabetic mice. These results suggest that naloxone-induced 'paradoxical' analgesia in mice may be mediated predominantly by delta-opioid receptors.
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PMID:Paradoxical analgesia produced by naloxone in diabetic mice is attributable to supersensitivity of delta-opioid receptors. 145 Sep 2

Opioid antagonists have been shown to produce dose-dependent analgesia in the formalin test in BALB/c mice. In light of this paradoxical finding, the motivational-affective property of naloxone was examined in BALB/c mice. Naloxone produced a conditioned place aversion at doses which were also found to produce analgesia in the formalin test (1 and 10 mg/kg). In addition, the analgesia produced by 1 mg/kg naloxone was completely abolished in mice pretreated with nor-binaltorphimine, a highly selective kappa-opioid antagonist. Norbinaltorphimine on its own, however, had no effect. These results suggest that the analgesic actions of naloxone may be due to an interaction with kappa receptors.
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PMID:Analgesic and aversive effects of naloxone in BALB/c mice. 149 94

Thirty elderly patients undergoing major hip surgery under spinal analgesia were randomly allocated in a double-blind manner into three groups. The aim was to evaluate the influence of intrathecal morphine and postoperative naloxone infusion on the regulation of ventilation. The Bupivacaine Group received spinal analgesia with 20 mg bupivacaine intrathecally. The Morphine Group received spinal analgesia with 20 mg bupivacaine + 0.3 mg morphine intrathecally. The Naloxone Group received spinal analgesia with 20 mg bupivacaine + 0.3 mg morphine intrathecally + postoperative naloxone infusion intravenously (1 microgram/kg/h over 12 h, 0.25 micrograms/kg/h over the next 12 h). Evaluation of resting ventilation and the ventilatory responses to hypercarbia and hypoxaemia was made on three occasions: before surgery, and 8, and 24 h after the intrathecal injection. Intrathecal morphine had no significant effect on ventilatory regulation in elderly patients undergoing major hip surgery performed under bupivacaine spinal analgesia. Postoperative administration of opioids or sedatives after intrathecal morphine as well as postoperative blood loss associated with a fall in blood pressure appeared to increase the risk of developing respiratory depression. Naloxone infusion seemed to reduce the risk of developing respiratory depression. Furthermore, one third of the elderly had a poor response to hypoxaemia before surgery.
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PMID:Influence of intrathecal morphine and naloxone intervention on postoperative ventilatory regulation in elderly patients. 163 66

We attempted to reverse the behavioral and neuronal antinociceptive effects of cocaine with naloxone, an opioid antagonist. Cocaine (20 mg/kg i.p.) produced a strong analgesic effect in the formalin test and in the tail pinch test. These cocaine-induced analgesic effects could be reversed by naloxone at a very high dose (10 mg/kg) but not at a dose (1 mg/kg) which was sufficient to attenuate morphine (10 mg/kg)-induced analgesia. Naloxone alone at a dose of 10 mg/kg did not produce significant effects. In general, nociceptively evoked responses in medial thalamic neurons were suppressed by cocaine (20 mg/kg), and this suppression was attenuated by naloxone (10 mg/kg). The results suggest that opioid receptors which are not involved in mediating morphine-induced analgesia and which have a low sensitivity to naloxone are involved in cocaine-induced central analgesia.
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PMID:Attempted reversal of cocaine-induced antinociceptive effects with naloxone, an opioid antagonist. 164 16

Chronic opioid antagonist administration increases opioid binding sites and potentiates behavioral responses to morphine. The present study was designed to examine in rats the temporal and dosage parameters of naloxone-induced potentiation of morphine analgesia and the effect of continuous infusion of naloxone on the analgesic potency of other mu agonists. Cumulative dose-response curves were generated in a tail-flick procedure for each drug tested. Naloxone-filled osmotic pumps were then implanted s.c. for 1 week after which the rats were retested with the agonist. The potency ratio of morphine (ED50 before naloxone/ED50 after naloxone) showed orderly increases over a range of naloxone doses (0.03-1.0 mg/kg/hr) and increased, then decreased, over a range of time points (6-72 hr) after removal of the osmotic pumps. The relative potency of morphine was 2.1 at 24 hr after a 7-day infusion of 0.3 mg/kg/hr of naloxone. These parameters were then used in tests of other mu agonists. Five drugs produced maximum increases in tail-flick latencies before naloxone. Of these, naloxone increased the analgesic potency of fentanyl, methadone and levorphanol (relative potencies ranged from 1.7-2.1) but not of etorphine and propoxyphene. The naloxone infusion increased the maximum analgesic effect of meperidine, profadol and pentazocine, but had no effect on the analgesic activity of buprenorphine, butorphanol, ethylketocyclazocine and nalbuphine. Our results demonstrate that 7-day naloxone infusion increases the analgesic potency of some, but not all, opioids with mu agonist activity.
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PMID:Increased analgesic potency of mu agonists after continuous naloxone infusion in rats. 165 5

Self-aggression is a behavioural disorder in which an individual damages its own body parts by intense biting or scratching. Self aggression has been reported in human patients in Lesch-Nyhan syndrome and in cases of schizophrenia, depression, and congenital analgesia. In human patients as well as in experimental animals some kind of dysesthesia of the part of the body that is mutilated has been suggested. This study was conducted to find out the underlying pain mechanisms in self-aggressive behaviour arising out of stereotypy. The study was performed in 40 adult male rats. In all these animals, self-aggression was produced as part of amphetamine induced stereotyped behaviour. A predetermined scale was used for quantifying this behaviour. Reserpine and phenoxybenzamine pretreatment led to an increase in the incidence of self-aggression. Naloxone administration in reserpine pretreated animals led to a further significant increase in the incidence of self biting as compared to controls. From these studies it appears that self-aggressive behaviour may be associated with increased pain sensation.
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PMID:Role of opioid receptors in self-aggression in rats. 166 47

Alpha 2-Adrenoceptors mediate analgesia in vivo. The present study explored the actions of the alpha 2-adrenoceptor agonists dexmedetomidine and clonidine on a nociceptive response in isolated neonatal rat spinal cord. Stimulation of a dorsal root generates a slow ventral root potential (slow VRP) at the corresponding ipsilateral ventral root. The slow VRP meets several criteria for a nociceptive response. Dexmedetomidine (10 nM) and clonidine (200 nM) depressed the slow VRP by approximately 80%. Dexmedetomidine's action was approximately linear over the concentration range 0.5-500 nM, whereas clonidine (20 nM-5 microM) exerted biphasic effects. The profile of agonist and antagonist effectiveness characterized the receptor(s) as alpha 2-adrenoceptors; the subtype could not be identified as either alpha 2A or alpha 2B. Naloxone pretreatment partially blocked dexmedetomidine's effect, suggesting a possible endogenous opiate involvement. Dexmedetomidine (0.5-2.0 nM) also depressed the VRP evoked by application of substance P to the cord, implicating postsynaptic as well as possible presynaptic actions. At high concentrations, dexmedetomidine (50-500 nM) depressed the monosynaptic reflex, probably through non-alpha 2-receptor(s). Results from the neonatal spinal cord correlate well with those from in vivo analgesia studies. They suggest an important direct spinal contribution to alpha 2-adrenoceptor-mediated analgesia.
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PMID:Alpha 2-adrenoceptors inhibit a nociceptive response in neonatal rat spinal cord. 167 74

A case of respiratory depression which occurred following administration of epidural meperidine during Caesarean section is described. Epidural meperidine, 75 mg (10 mg.ml-1) was given after delivery of the infant to provide postoperative analgesia. Oxygen desaturation (SaO2 90%) and a decrease in respiratory rate (4.min-1) were noted 30 min after epidural meperidine was administered. Naloxone, 0.1 mg, was given iv which resulted in prompt improvement in both respiratory rate and oxygen saturation. Vascular absorption of meperidine from the epidural venous plexus is the most probable explanation for this case of early respiratory depression. We recommend a maximum bolus dose of 50 mg of epidural meperidine for pain management after Caesarean section. It is also important to monitor oxygen saturation continuously during the intraoperative period, and to monitor the patient closely in the recovery room for at least one hour for evidence of respiratory depression.
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PMID:Early respiratory depression during caesarean section following epidural meperidine. 173 38


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