Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
 ...
PMID:[Psychophysiology of fire walking. II. Pain perception in pyrovasy (fire walking)]. 49 16

Pain evoked potentials (EPs) were recorded in nucleus caudatus (NC) of rabbits after electric stimulation of the dental pulp. After 50--60 noxious stimuli the decrease in amplitude of evoked potentials occured. Naloxone, 1 mg/kg, temporarily abolished this effect and even after 350 noxious stimuli the habituation was not observed. On the other hand, naloxone did not affect the diminution of monosynaptic transcallosal potentials (TC--EP) evoked by repeated stimulation. It may be suggested that the habituation of EPs elicited by pain stimulation is due to endorphin release.
 ...
PMID:Lack of habituation of pain evoked potentials after naloxone. 50 69

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.
 ...
PMID:2-Deoxy-D-glucose analgesia: influences of opiate and non-opiate factors. 50 9

The conditioned taste aversion paradigm (CTA) was used to examine the effects of naloxone on ethanol-induced aversion towards a saccharine solution (3 conditioning and 11 extinction trials). Six groups of rats received conditioning trials consisting of two IP injections after saccharine presentation of different combinations of either ethanol (E: 1.75 g/kg), LiCl (L: 12 mEq/kg, 0.1 M), naloxone (N: 10 mg/kg) or saline (S); S-S, S-N, E-S, E-N, L-S and L-N. Naloxone by itself produced no aversion to the saccharin flavor. Based on the onset and extinction of aversion, naloxone significantly enhanced ethanol but also LiCl-induced CTA. The comparative data argues in favor of different mechanisms of action (1) between the aversive central effects of ethanol and morphine and (2) between ethanol's acute behavioral effects and negatively reinforcing properties. Enhancement of ethanol and LiCl-induced CTA by naloxone is compatible with hypernociceptive action of the opiate-antagonist and with the pain-modulating role of opiates in the CNS.
 ...
PMID:Non-specific enhancement of ethanol-induced taste aversion by naloxone. 52 97

Clonidine was found to possess dose-dependent analgesic and antiwithdrawal activity. In mice, clonidine prolonged the tail flick latency and inhibited phenylquinone-induced writhing. In rats, it inhibited tail withdrawal from hot water and a pain response to pressure application on an inflamed paw. The effective doses of clonidine were different in the different tests employed, but they were always smaller than those of morphine. Naloxone failed to antagonize the analgesic actions of clonidine but effectively antagonized those of morphine. Phenoxybenzamine also did not alter the inhibition of tail flick-induced by clonidine. Clonidine suppressed morphine withdrawal body shakes in a dose-dependent manner as does morphine. This action of clonidine was not reversed by naloxone. In usual laboratory tests, clonidine appears to be an effective analgesic which antagonizes signs of morphine withdrawal.
 ...
PMID:A comparison of clonidine with morphine for antinociceptive and antiwithdrawal actions. 56 95

74 patients, undergoing gynaecological operations under neuroleptanesthesia were subdivided into 4 groups, each receiving Naloxone in different doses postoperatively. For a longer period of time tidal volume, respiratory rate, minute ventilation, blood gas volues and pain index were recorded. From the results one can conclude that 0.1-0.2 mg Naloxone i.v. seems to be the most effective dose to reverse opiate-induced respiratory depression. The initial i.v. dose should be followed by an i.m. dose of 0.2 mg, if required.
 ...
PMID:[Changes of the blood gases following the application of naloxon (author's transl)]. 84 13

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.
 ...
PMID:Nitrous oxide analgesia: reversal by naloxone and development of tolerance. 92 57

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.
Pain 1992 Jul
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.
Pain 1992 Jun
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 effect of the presence of either chronic or acute clinical pain on pain threshold and on the nociceptive flexion reflex (RIII) threshold was studied. The experimental pain sensation and the flexion reflex were evoked by trains of short electrical pulses. It was hypothesized that both kinds of clinical pain would be able to induce 'diffuse noxious inhibitory controls' (DNIC) and thereby raise the 2 experimental thresholds. Patients with chronic low back pain, patients with postoperative pain from oral surgery, and pain-free subjects were tested in 3 conditions: during baseline, after i.v. administration of a placebo, and after i.v. administration of naloxone. In comparison with 2 pain-free control groups, the 2 pain groups had a significantly higher pain threshold in all conditions. However, the RIII threshold was not significantly elevated in chronic or acute pain patients compared to controls. Naloxone had no effect on the RIII or pain threshold in any of the groups. It is concluded that the increased pain threshold which is frequently found in chronic pain patients, and which could be confirmed in the present study, does not result from a DNIC effect. The adaptation level theory offers an alternative explanation. Also, the acute postoperative pain in this study did not seem to induce DNIC. Because other forms of acute pain have been found to be effective in activating DNIC, future research should establish which pains are and which pains are not effective.
Pain 1992 Aug
PMID:Chronic back pain, acute postoperative pain and the activation of diffuse noxious inhibitory controls (DNIC). 140 14


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>