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Query: UMLS:C0184567 (acute pain)
 3,962 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Chronic back pain, acute postoperative pain and the activation of diffuse noxious inhibitory controls (DNIC). 140 14

The reliability of some behavioral and physiological indices used for the recognition and assessment of acute pain in lambs after castration and tail docking has been examined. Changes in the indices were measured after blocking neural activity with local anaesthetic (lignocaine) and after an opioid antagonist (naloxone) was administered. Six lambs, aged less than one week, were allocated randomly to each of six treatments. (i) control handling and blood sampling; (ii) castration plus tail docking with tight rubber rings; (iii) local anaesthesia; (iv) local anaesthesia followed by castration and tail docking; (v) intravenous naloxone only (0.2 mg kg-1); and (vi) intravenous naloxone followed by castration and tail docking. Local anaesthesia eliminated the behavioural and plasma cortisol changes which usually follow castration and tail docking. Naloxone had a limited effect on the increase in cortisol but altered the behaviour. The results support the view that such indices are useful for assessment of the response to acute pain and that, although endogenous opioids do reduce pain in young lambs after castration and tail docking, the effect is small.
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PMID:Effects of local anesthesia and intravenous naloxone on the changes in behaviour and plasma concentrations of cortisol produced by castration and tail docking with tight rubber rings in young lambs. 178 83

Naloxone per se causes no pain in normal man, indicating that opioidergic antinociceptive systems are not tonically active, but this might not be the case in chronic pain conditions. The present investigation tested the hypothesis that pain in chronic headache is the result of insufficiently attenuated nociceptive impulses. Forty-seven patients suffering from chronic tension headache entered the present double-blind cross-over trial of naloxone 4 mg i.v. versus saline. Adverse effects were negligible. Patients scored headache pain on a 100 mm visual analog scale and change in headache on a 5-point verbal rating scale after 5, 15, 30, 60 and 90 min. Mean arterial blood pressure decreased 4.2 mm Hg (P less than 0.05) after naloxone compared to saline, but naloxone had no effect on headache (P = 0.96). A bimodal distribution of acute pain patients into placebo responders and non-responders has been reported, but our chronic pain patients showed a homogeneous placebo response. Review of the literature indicates that acute clinical pain and stimulation-induced analgesia in experimental pain has a naloxone-responsive component. Chronic pain does not appear to be influenced by naloxone in moderate doses.
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PMID:Naloxone in moderate dose does not aggravate chronic tension headache. 268 74

On the basis of data obtained from subprimates subjected to acute pain stimuli, it has been hypothesized that the suppression of chronic pain in man during stimulation in the periventricular region involves endogenous opioid mechanisms. However, there is at present no direct and unequivocal proof that the pain relief in man is necessarily and entirely dependent upon such mechanisms. There exist several putative substances with opiate-like properties but they are difficult to identify. The assay methods lack specificity and cross-reactions are common. There are only a few studies published on the influence of intracerebral stimulation in man on the CSF-content of opioid substances; the changes observed are inconsistent, and data are only given on patients having satisfactory pain relief. Furthermore, measurements have been made only during the course of a few hours and nothing is reported on the relationship between the changing concentrations of the substance and the level of pain. The observation that Naloxone may reverse the effect of intracerebral stimulation has become the keystone in postulating common mechanisms for stimulation-produced pain relief and morphine analgesia. The fact, that Naloxone is sometime ineffective or has to be used in huge, and unphysiological, doses is generally disregarded. There are a number of substances which may serve as neurotransmittors in pain transmission and pain inhibition but their mode of action in the generation and suppression of chronic pain is entirely unknown. Data collected from various European clinics covering more than 200 patients subjected to intracerebral stimulation show that the outcome of this treatment is highly unpredictable. Intracerebral stimulation as a clinically useful treatment of chronic pain can not be further developed unless hard data on its biochemical background in man are provided.
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PMID:Biochemistry of pain relief with intracerebral stimulation. Few facts and many hypotheses. 625 3

1. Various clinical and experimental reports indicate that tricyclic antidepressant drugs are specially useful in the treatment of chronic and acute pain conditions. The present work was aimed to study the mechanisms implicated in the antinociceptive response induced by these antidepressants on different experimental models of pain in mice, and particularly the role played by noradrenergic, serotonergic and opioidergic influences. 2. Electrical stimulation of the tail and formalin tests were used to evaluate pain perception in mice acutely treated with different antidepressants (imipramine, desipramine, amitriptyline, nortriptyline, clomipramine and desmethylclomipramine). Antinociceptive responses were more potent in formalin test than in tail electrical stimulation test. 3. These antinociceptive effects were inhibited by naloxone (2 mg/Kg, i.p.), alpha-methyl-p-tyrosine (200 mg/Kg) and p-chlorophenylalanine (600 mg/Kg). Naloxone elicited the same effectivity to inhibit antinociceptive responses induced by tricyclic antidepressants in both tail electrical stimulation and formalin tests. alpha-methyl-p-tyrosine and p-chlorophenylalanine were more effective on antinociceptive responses induced on formalin than in tail electrical stimulation test. 4. These results suggest that tricyclic antidepressants produce antinociception partly via the participation of the endogenous opioid system and partly by further activating noradrenergic and serotonergic pathways. Moreover, the analgesic responses and the mechanisms implicated were dependent of the analgesimeter test used.
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PMID:Participation of opioid and monoaminergic mechanisms on the antinociceptive effect induced by tricyclic antidepressants in two behavioural pain tests in mice. 782 61

Systemic and intrathecally administered ketorolac produced antinociception in the p-phenylquinone test, but not in the tail-flick or hot-plate tests. Antagonists of the subtypes of opioid receptors were used to evaluate the interaction of ketorolac with these receptors. Intrathecally administered kappa-opioid receptor antagonist nor-binaltorphimine dihydrochloride blocked the antinociceptive effects of systemic ketorolac and intrathecally administered ketorolac. Naloxone and ICI 174,864 failed to block the effects of ketorolac. Activation of nor-binaltorphimine-sensitive receptors appears to be an integral element in the mechanism of antinociception of ketorolac at the spinal level. Ketorolac did not precipitate withdrawal jumping in morphine-tolerant mice demonstrating that ketorolac does not act as a mixed agonist-antagonist at the opioid receptor. We suggest that neuraxial placement of ketorolac may prove useful in the clinical setting for the management of acute pain in humans.
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PMID:Antinociceptive activity of intrathecal ketorolac is blocked by the kappa-opioid receptor antagonist, nor-binaltorphimine. 822 36

1. We evaluated the ability of the functional antagonist at the glycine site of the N-methyl-D-aspartate (NMDA) receptor complex, (+)-(1-Hydroxy-3-aminopyrrolodine-2-one) ((+)-HA966), to modulate the antinociceptive action of systemic morphine in a rat model of neuropathic pain produced by chronic constriction injury to the sciatic nerve. Mechanical (vocalization threshold to hindpaw pressure) and thermal (struggle latency to hindpaw immersion into a water bath) stimuli were used. 2. In the mechanical test, morphine (0.05, 0.1 and 0.3 mg kg(-1), i.v.) alone produced dose-dependent effects in both neuropathic and uninjured rats. Likewise, morphine (0.1, 0.3 and 1 mg kg(-1), i.v.) dose-dependently increased struggle latencies of the nerve-injured hindpaw in the hot noxious (46 degrees C) test but was ineffective in the non-noxious warm (44 degrees C) and cold (10 degrees C) test. 3. Pretreatment with (+)-HA966 (2.5 mg kg(-1), s.c.) dose-dependently enhanced the effect of morphine in the mechanical test with the relative potency being nerve-injured hindpaw > contralateral hindpaw > uninjured rat. 4. Likewise, (+)-HA966 dose-dependently enhanced the effect of morphine against a hot (46 degrees C) stimulus and produced, in combination with morphine, a dose-dependent effect against a warm (44 degrees C) stimulus. In the cold (10 degrees C) test, (+)-HA966 reversed the ineffectiveness of the highest dose of morphine. 5. Naloxone blocked the effect of the combination of (+)-HA966 with morphine in all tests. The drug combination produced no motor deficits in animals using the rotarod test. 6. These findings suggest that combined administration of antagonists, acting at the glycine site of the NMDA receptor complex and morphine may be a promising approach in the treatment of neuropathic and acute pain.
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PMID:The antinociceptive effect of combined systemic administration of morphine and the glycine/NMDA receptor antagonist, (+)-HA966 in a rat model of peripheral neuropathy. 988 55

The aim of this study was to investigate the neurotransmissions involved in the antinociceptive effect of tramadol in the formalin test, which is an animal model of acute and tonic pain. A subcutaneous injection of formalin produces a biphasic nociceptive response: phase 1 (0-10 min-acute pain) and phase 2 (21-60 min-tonic pain). Nociceptive activity is reduced greatly during the 10 min between these two phases. We measured in mice the effects of (+/-)-tramadol, and of (+)- and (-)-tramadol administered before the induction of pain by formalin, in the presence and absence of drugs that act on the opioidergic, serotonergic and noradrenergic systems (naloxone, ketanserin, fluoxetine, maprotiline). With respect to animals treated with formalin alone, (+/-)-tramadol and its enantiomers significantly reduced the duration of nociceptive behaviours (lifting, licking, favouring, shaking, and flinching of the formalin-treated paw) during phase 2. This effect was prevented by the 5-HT(2) receptor antagonist ketanserin, but not by naloxone which, on the contrary, was able to prevent the antinociceptive effect of morphine. Naloxone and ketanserin did not affect the duration of nociceptive behaviour in animals not treated with tramadol. Fluoxetine (a selective 5-hydroxytryptamine (5-HT) reuptake inhibitor), but not maprotiline (a selective norepinephrine reuptake inhibitor), potentiated the antinociceptive effect of (+/-)-tramadol. In conclusion, we demonstrate that the serotonergic pathway is responsible for the antinociceptive effect of tramadol in phase 2 of the formalin test, and that this effect is mediated by 5-HT(2) receptors.
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PMID:The antinociceptive effect of tramadol in the formalin test is mediated by the serotonergic component. 1207 82

Triterpenoid saponins from Stauntonia chinensis (TSS) are potential therapeutic agents because of its analgesic properties. However, the underlying mechanisms of the anti-nociceptive activity of TSS are largely unclear, especially in CNS. The present study confirmed the analgesic effect of TSS using four models of acute pain based on thermal or chemical stimuli. TSS treatment specifically impaired the threshold of thermal- and chemical-stimulated acute pain. Naloxone did not block the anti-nociceptive effects of TSS, which showed no participation of the opioid system. We investigated the electrical signal in cultured cortical neurons to explore whether TSS treatment directly affected synaptic transmission. TSS treatment selectively increased spontaneous inhibitory synaptic release and GABA induced charge transfer in mouse cortical neurons. The effects of TSS were maintained for at least 8 h in cultured neurons and in injected mice. Taken together, our results suggest that the analgesic role of TSS in cortex occurs via a particular increase in the inhibitory synaptic response at resting state, which supports TSS as a potential candidate for inflammatory pain relief.
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PMID:Analgesic Effects of Triterpenoid Saponins From Stauntonia chinensis via Selective Increase in Inhibitory Synaptic Response in Mouse Cortical Neurons. 3048 36

Opioids are not first-line therapy for chronic noncancer pain or nonsevere acute pain. Overall, evidence does not show that opioids are superior to nonopioid interventions, and opioids pose a high risk of harm. A trial of opioid therapy may be considered for patients who have persistent severe pain plus functional limitations despite adherence to multiple appropriate nonopioid therapies. Individual benefits and harms, including potential adverse effects, overdose risk, and opioid use disorder risk, must be assessed thoroughly before opioid therapy is initiated. A trial period of opioid therapy should be established using immediate-release formulations at low doses. Multimodal management with nonopioid therapies should be continued. Strategies for mitigating risk with long-term opioid use include regular follow-up review of benefits and harms, use of prescription drug monitoring programs, urine drug screenings, and opioid treatment agreements. Caution is indicated when 50 or more morphine milligram equivalents (MME)/day of opioids are prescribed, and dosages of 90 MME/day or more should be avoided. Naloxone should be provided for patients at high risk of overdose. If harms outweigh benefits, opioids should be tapered and discontinued.
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PMID:Prescription Drug and Alcohol Use Disorders: Safe Prescribing of Opioids. 3084 20


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