Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

On six occasions spaced at least a week apart, two groups of rats were subjected to a variety of stressful conditions consisting of a restraint/bright light complex, either alone or in combination with a tail pinch, whole-body inversion, or partial immersion in cold water. One of these groups was injected with diazepam (2.0 mg/kg) 30 min prior to the stressors, while the other group experienced the drug in their home cages the following day. A third group also received the diazepam but was not exposed to the stressors. In three test sessions all animals were injected with either diazepam or saline and were then exposed to a novel stressor: a plus-maze used as a screening device for anxiolytic drugs. This was immediately followed by a tail-flick measure of analgesia. The longest tail-flick latencies, indicating stress-induced analgesia ("autoanalgesia"), were observed in the group that had not been exposed to stress prior to testing. The other two groups exhibited substantially shorter latencies but did not differ from one another, thus showing a "stress inoculation" effect that was uninfluenced by diazepam. In the plus-maze, diazepam tends to increase the amount of time rats will spend in the two exposed arms of the maze relative to the two enclosed arms. This effect was significantly attenuated in the group that had previously experienced the variety of stressors after a diazepam injection, suggesting a learned association between drug and stress that resulted in a diminution of the drug's anxiolytic property.
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PMID:Diazepam-stress interactions in the rat: effects on autoanalgesia and a plus-maze model of anxiety. 233 Dec 32

Ninety-six Ss rated pain during baseline and posttreatment exposures to cold pressor pain. Between trials, Ss in four groups were trained to use one of four cognitive coping strategies involving (a) imaginal reinterpretation, (b) imaginal distraction, (c) nonimaginal reinterpretation, or (d) nonimaginal distraction. Two additional groups were given: (e) an expectation for analgesia but no coping strategy and (f) no treatment. The four coping strategies produced equivalent attenuation of pain ratings and equivalent expectancies for analgesia. Expectancy control Ss expected analgesia, but reported no significant pain reductions. No treatment control Ss neither expected nor achieved any significant pain reductions. Among cognitive strategy groups, the Ss absorption added significantly to the variance in pain reduction above and beyond the effects of expectancy. Theoretical implications are discussed.
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PMID:Effectiveness of maximally different cognitive strategies and expectancy in attenuation of reported pain. 234 63

The role of neural histamine in morphine-analgesia and in morphine-induced potentiation of stress analgesia was studied. Pretreatment of rats with alpha-fluoromethylhistidine (alpha-FMH) (200 micrograms i.c.v./rat; daily for five days) increased the analgesic potency of morphine, centrally or peripherally injected, in the tail-flick assay. This increase was significantly blocked by i.c.v. or i.p. beta-funaltrexamine (beta-FNA) a mu selective irreversible opioid receptor antagonist, whereas i.c.v. injected naltrexone did not block the increased analgesic potency of the i.c.v. morphine. Rats subjected to cold-restrained stress (60 min at 4 degrees C) showed increased tail-flick latency, compared to the unstressed group. The analgesic potency of morphine was significantly greater in rats subjected to restraint with respect to unstressed rats. However, the inhibition of histamine biosynthesis by alpha-FMH significantly reduced cold-restraint analgesia in controls, and also inhibited the analgesic efficacy of the opiate. These results indicate that neural histamine may be responsible for pain response modifications observed in rats subjected to cold-restraint conditions, and of morphine-potentiation of stress analgesia. The data also suggest a close association between increased analgesic potency of morphine and inhibition of histaminergic effects, possibly implying a functional supersensitivity and an increase in opioid receptors.
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PMID:Peripheral and central opioid activity in the analgesic potency of morphine. 237 23

In the present experiments the role of unmyelinated sensory fibres in the mechanism of cutaneous inflammatory reactions under normal and pathological conditions has been studied in man and animals. Dye leakage responses to histamine, serotonin, compound 48/80, bradykinin and substance P were significantly reduced, while neurogenic inflammation was completely abolished in rats treated neonatally with capsaicin, as studied quantitatively by the Evans blue technique. Neurogenic inflammation could also be elicited by mustard oil in normally innervated human skin, but not in skin areas affected by herpes zoster or in a patient suffering from congenital analgesia. Repeated topical treatment of the skin with capsaicin (local desensitization) abolished the neurogenic inflammatory response for several days. Chemical pain sensitivity was strongly reduced, and thresholds for warmth and heat pain sensations were significantly elevated. Local capsaicin desensitization of the skin prevented whealing, flare and itch in patients with acquired cold and heat urticaria. The findings indicate that peptide-containing sensory nerves are involved in the mediation of chemogenic and heat pain, and possibly itch, and are responsible for initiation of the neurogenic inflammatory response. The results also provide direct evidence of the involvement of these particular sensory nerves in the modulation of the permeability-increasing effects of putative mediators of acute inflammatory reactions. It is concluded that, through modulation of cutaneous vascular reactions, peptidergic sensory nerves may play a hitherto unrecognized role in the pathomechanism of certain diseases of human skin.
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PMID:The modulation of cutaneous inflammatory reactions by peptide-containing sensory nerves. 241 73

1. The terrestrial snail, Cepaea nemoralis, when placed on a warmed surface (40 degrees C) displays a thermal avoidance behaviour that entails an elevation of the anterior portion of the fully extended foot. The latency of this nociceptive response was increased by the prototypical mu and specific kappa opiate agonists, morphine and U-50, 488H, respectively, in a manner indicative of anti-nociception and the induction of 'analgesia'. Pretreatment with the prototypical opiate antagonist, naloxone, blocked the morphine- and reduced the U-50, 488H-induced analgesia. Naloxone had no effects on the thermal response latencies of saline treated animals. 2. Exposure to either cold (7 degrees C) or warm (38 degrees C) temperature stress increased the nociceptive thresholds of Cepaea in a manner indicative of the induction of 'stress-induced analgesia'. The warm stress-induced analgesia was opioid mediated, being blocked by naloxone, whereas, the cold stress-induced analgesia was insensitive to naloxone. 3. Exposure for 15-30 min to 0.5 Hz weak rotating magnetic fields (1.5-8.0 G) significantly reduced the analgesic effects of the mu and kappa opiate agonists in a manner similar to that observed with naloxone. The magnetic stimuli also inhibited the endogenous opioid mediated warm stress-induced analgesia and significantly reduced the cold stress-induced analgesia. The magnetic stimuli had no evident effects on the nociceptive responses of saline-treated animals. The dihydropyridine (DHP) and non-DHP calcium channel antagonists diltiazem, verapamil. and nifedipine differentially and significantly reduced, while the DHP calcium channel agonist, BAY K8644, significantly enhanced the inhibitory effects of the magnetic fields on morphine-induced analgesia.
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PMID:Magnetic fields inhibit opioid-mediated 'analgesic' behaviours of the terrestrial snail, Cepaea nemoralis. 245 51

Alterations in nociceptive reactivity, opiate receptor binding, and other behavioral responses occur in rats exposed to morphine either in utero or post-natally. The present study examined whether post-natal morphine (0, 1 or 20 micrograms, days 1-7) altered analgesia on the tail-flick and jump tests induced by nonopioid-mediated continuous cold-water swims (CCWS), opioid-mediated intermittent cold-water swims (ICWS) or morphine (2.5 and 5.0 mg/kg, SC) in adult male and female rats. Changes in body weight, developmental signs (e.g., eye opening), basal pain thresholds, and both CCWS and ICWS hypothermia were also assessed. Previously-reported gender differences occurred for all forms of analgesia in control rats. Post-natal morphine treatment transiently increased ICWS analgesia and hypothermia, and transiently decreased CCWS analgesia and hypothermia, suggesting that these effects were not specific to pain inhibition. Post-natal morphine treatment significantly increased the magnitude of morphine analgesia on both tests in females, and significantly decreased the magnitude of morphine analgesia on both tests in males, thereby acting to vitiate the observed gender differences in morphine analgesia. Such effects could not be explained by concomitant changes in other measures. These data indicate that post-natal morphine treatment exerts highly selective effects upon specific analgesic responses which are gender sensitive.
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PMID:Post-natal morphine differentially affects opiate and stress analgesia in adult rats. 250 92

A lot of researches indicate that central nervous system not only exist endogenous opiate analgesic system but also possess endogenous nonopiate analgesic system. The opiate and nonopiate analgesic systems can be selectively activated by different environmental or artificial manipulations and modulated the stimulation-produced analgesia, acupuncture analgesia and stress-induced analgesia, including the foot shock-induced analgesia, tail-shock-produced analgesia, ear-shock-induced analgesia, analgesia of cold water swim, analgesia of immobilization or of restraint and analgesia of a-Deoxy-D- glucose and so on. The existence and description of these modulatory mechanisms have it's multiplicity and important clinical implications for the treatment of pain.
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PMID:[The endogenous opiate and nonopiate analgesic system]. 251 18

A study has shown that, when applied to Physalia ("bluebottle") jellyfish stings, cold packs are effective as topical analgesia in the relief of mild-to-moderate skin pain. The application of ice also has been shown to be effective for topical analgesia in a number of other jellyfish stings, including by Cyanea ("hair jellyfish"), Tamoya sp. ("Moreton Bay stinger" or "fire jelly") and Carybdea rastoni ("jimble") as well as by Physalia. In the current state of knowledge, cold packs or ice are recommended as the first-aid treatment for jellyfish stings with local skin pain.
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PMID:Cold packs: effective topical analgesia in the treatment of painful stings by Physalia and other jellyfish. 257 8

The efficacy of transcutaneous electrical nerve stimulation (TENS) in producing analgesia in cold-induced pain was assessed using a range of 5 stimulating frequencies (10 Hz, 20 Hz, 40 Hz, 80 Hz and 160 Hz) in 83 normal healthy subjects. TENS significantly elevated ice pain threshold when compared with sham and control groups. TENS frequencies between 20 and 80 Hz produced greatest analgesia, while frequencies below and above this level (10 Hz and 160 Hz), although significantly elevating ice pain threshold, produced effects of a lesser magnitude. The frequency of pulse delivery was the governing factor as no significant differences in stimulus intensity were observed across the treatment groups. Measurement of ice pain tolerance was found to be unreliable under the present conditions. No significant relationships were observed between personality variables as measured by Eysenck Personality Questionnaires and the degree of TENS response.
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PMID:Analgesic effects of different frequencies of transcutaneous electrical nerve stimulation on cold-induced pain in normal subjects. 259 1

Neonatal administration of monosodium glutamate (MSG: 2-4 mg/g, SC) selectively destroys circumventricular organs, especially the arcuate nucleus and median eminence of the hypothalamus, and also attenuates both nonopioid (continuous cold-water swim: CCWS) and opioid (morphine) analgesia when rats are tested as adults. The present study evaluated whether administration of MSG (1-6 g/kg, SC) or its equiosmotic control (2.37 M NaCl) to adult rats altered either basal nociception on the tail-flick and jump tests or analgesia following morphine (5 mg/kg, SC) or CCWS (2 degrees C for 3.5 min). MSG treatment dose-dependently produced small but significant increases in basal nociceptive thresholds in adult rats. Morphine analgesia was significantly reduced on both tests following pretreatment with MSG (30-32%) and hypertonic NaCl (17-25%). In contrast, MSG (55-247%), but not NaCl pretreatment potentiated both nonopioid CCWS analgesia on both tests and CCWS hypothermia. These data are discussed in terms of differential neonatal and adult MSG effects, dissociations between opioid and nonopioid pain-inhibition, and the role of MSG in altering adaptive mechanisms to environmental stressors.
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PMID:Dissociation of opioid and nonopioid analgesic responses following adult monosodium glutamate pretreatment. 260 62


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