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)

1. Dexamethasone or RU 38486 were administered intraperitoneally or intracerebroventricularly to mice 10 or 120 min before morphine administration. The interaction of these drugs with the analgesic effects of morphine was examined using the hot plate test. 2. Dexamethasone i.p. pretreatment reduced analgesic responses to morphine injected 120 min but not 10 min after dexamethasone; i.c.v. injection of dexamethasone 10 and 120 min before morphine administration was effective in reducing morphine analgesia. 3. RU 38486 i.c.v. pretreatment (but not i.p. pretreatment) performed 120 (but not 10) min before morphine administration enhanced morphine analgesic effects. 4. These results, particularly the effects of drug interaction for i.c.v. administration, strongly confirm a central site for dexamethasone and RU 38486 action.
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PMID:The interaction of peripherally and centrally administered dexamethasone and RU 38486 on morphine analgesia in mice. 176 Nov 97

The effect of dexamethasone on exercise-induced adrenocorticotropin (ACTH) secretion and dental analgesia was studied in healthy human subjects. Different levels of exercise (100-200 W) were produced by a cycle ergometer. Dental pain thresholds were tested with a constant current stimulator. Dental pain thresholds were elevated with increasing work loads, and the elevation was still significant 30 min after the end of the exercise. Dexamethasone produced a significant reversal of exercise-induced pain threshold elevations concomitantly with the suppression of exercise-induced ACTH release. The results suggest that the corticotropin releasing factor-ACTH axis is involved in the exercise-induced analgesia.
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PMID:Dexamethasone attenuates exercise-induced dental analgesia in man. 216 84

Many reports have indicated that electro-acupuncture analgesia (EAA) was mediated by endorphins. Among them is B-endorphin which can be released from the anterior lobe of the pituitary. To examine the role of B-endorphin in EAA and observe CNS metabolic (functional) and behavioral effects of dexamethasone the present study employed the (14C) 2-deoxyglycose (2DG) method. Seventeen adult male Sprague-Dawley rats in five groups received the following different types of somesthetic stimulation to examine the local cerebral glucose utilization (LCGU) and tail-flick response latency: control group (N = 3), pain group (N = 4), EA group (N = 3), pain + EA group (N = 3; from another ongoing study) and dexamethasone group (N = 4). Dexamethasone reduced tail-flick response latency in response to electroacupuncture, and produced metabolic (functional) changes in a number of CNS structures implicated in electroacupuncture produced analgesia effects (some changes were statistically significant, many others were not). Specific brain structures exhibiting statistically significant changes (p less than 0.05) in LCGU when compared to the pain + EA group are: the parafascicular and habennlar nuclei of the thalamus and the posterior cingulate gyrus. In comparison of dexamethasone group with the other four experimental groups of rats, the following trend in LCGU changes was observed: pain + EA group greater than pain group = EA group = dexamethasone group greater than control group. In addition, dexamethasone had a sedative effect. The results suggest that dexamethasone is reducing EAA and having suppressive effects on CNS metabolism and behavior.
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PMID:Effects of dexamethasone on electroacupuncture analgesia and central nervous system metabolism. 289 1

A 24-year-old black female presented for repeat elective Caesarean section. The procedure was performed under epidural anaesthesia. Sufentanil 25 micrograms, intended for postoperative analgesia, was inadvertently diluted to 10 ml with 15 per cent potassium chloride (KCl) instead of preservative-free normal saline (0.9 per cent NaCl). This solution was then injected via an epidural catheter into the epidural space at the conclusion of surgery. Two hours after injection of the sufetanil-KCl mixture, the patient had a level of sensory blockade to T1 and diaphoresis above this level. Painful muscle spasms had also developed below T1. One hour later she developed hypertension which required hydralazine 10 mg and labetalol 25 mg IV for treatment. The patient was treated supportively with oxygen. Dexamethasone 10 mg was administered intravenously to reduce spinal cord oedema. Intravenous diazepam 10 mg and meperidine 75 mg were given for sedation and analgesia. Complete recovery occurred within 12 hours.
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PMID:Inadvertent epidural administration of potassium chloride. A case report. 297 23

The authors examine a technique that is performed for control of postoperative pain. Sixty-eight patients were evaluated who had received a combination of Marcaine with no epinephrine, plus Hexadrol, at the surgical site immediately postoperatively. It was found that 65% did not require any form of analgesia within the first 4 hours postsurgically; 44% the first 8 hours, and 28% the first 12 hours. Sixteen percent of the patients required no form of analgesia during their entire hospital stay.
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PMID:Control of postoperative pain in foot surgery using a combination of anesthetic and steroid for local infiltration. 361 26

The effect of long term ACTH treatment on some actions of morphine were studied. The effect of ACTH administration was compared to that induced by acute dexamethasone injection. ACTH caused a delayed inhibition of the morphine induced increase in growth hormone secretion demonstrable 24 hr after the last hormone injection. The morphine induced increase of striatal DOPAC (3,4-dihydroxyphenylacetic acid) content was also inhibited by ACTH treatment, however, neither the analgesia, nor the hypermotility caused by morphine were affected. Dexamethasone did not alter significantly the responsiveness to morphine. It is concluded that the prolonged exposure to ACTH presumably causes a corticosterone-mediated loss of responsiveness of functionally restricted opiate sensitive mechanisms in the central nervous system.
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PMID:Loss of sensitivity to morphine induced by prolonged ACTH treatment. 608 72

The effect of a naloxone or a dexamethasone pretreatment on the conditioned analgesia resulting from the exposure of rats to an experimental chamber repeatedly paired with a grid shock was investigated. Shock induced disruption of bar pressing activity was taken as a behavioral measure of pain responsiveness. It was found that a 6, but not a 3, mg/kg dose of naloxone i.p. is hyperalgesic in unconditioned rats and effectively antagonizes conditioned analgesia. Dexamethasone (up to a dose of 2 + 1 mg/kg i.p. 23 and 1 h prior) did not alter the pain responsiveness of unconditioned rats, but caused a dose dependent suppression of conditioned analgesia. These results are discussed in terms of an opiate pituitary mechanism subserving conditioned analgesia.
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PMID:Behavioral evidence for an opiate pituitary mechanism subserving conditioned analgesia. 631 29

The effects of 3 different non-noxious stressors on body temperature (Tb) were investigated in the rat: (1) loose restraint in cylinders, (2) removal of the rats from cylinders, exposure to a novel environment and replacement in cylinders, a stressor called here 'novelty', and (3) gentle holding of the rats by the nape of the neck. Loose restraint and 'novelty' produced hyperthermia. On the contrary, holding induced hypothermia. Hypophysectomy (HX) reduced basal Tb, abolished restraint hyperthermia and reduced both 'novelty' hyperthermia and holding hypothermia. Dexamethasone ( DEXA ) had no effect upon either restraint or novelty hyperthermia but reduced the hypothermia. Naloxone (Nx) produced a slight fall in basal Tb accounting for its reduction of restraint and 'novelty' hyperthermias ; it did not affect holding hypothermia. The inhibitory effects of HX suggest a participation of the pituitary in the hyperthermias ; the neurointermediate lobe would be involved as the hyperthermias were not affected by DEXA , which is known to block the stress-induced release of pituitary secretions from the anterior lobe but not from the neurointermediate lobe. In contrast, substances from the anterior lobe might participate in hypothermia due to holding since it is reduced by HX and DEXA . As to the effects of Nx, endogenous opioids would not be significantly involved in the thermic effects of the stressors used in this study; they might play, if any, only a minor role in the regulation of basal Tb. These results are compared with those previously obtained on nociception using the same non-noxious stressors. It emerges that, depending on the stressor, different types of association between thermoregulation and nociception may occur, i.e. hyperthermia with analgesia, hyperthermia with hyperalgesia and hypothermia with hyperalgesia.
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PMID:Regulation of body temperature and nociception induced by non-noxious stress in rat. 672 30

1. Endogenous corticosteroids and opioids are involved in many functions of the organism, including analgesia, cerebral excitability, stress and others. Therefore, we considered it important to gain information on the functional interaction between corticosteroids and specific opioid receptor subpopulations. 2. We have found that systemic administration (i.p.) of the potent synthetic corticosteroid, dexamethasone, reduced the antinociception induced by the highly selective mu agonist, DAMGO or by less selective mu agonists morphine and beta-endorphin administered i.c.v.. On the contrary dexamethasone exerted little or no influence on the antinociception induced by a delta 1 agonist, DPDPE and a delta 2 agonist deltorphin II. Dexamethasone potentiated the antinociception induced by the kappa agonist, U50,488. 3. In experiments performed in an in vitro model of cerebral excitability in the rat hippocampal slice, dexamethasone strongly prevented both the increase of the duration of the field potential recorded in CA1, and the appearance and number of additional population spikes induced by mu receptor agonists. 4. In both models pretreatment with cycloheximide, a protein synthesis inhibitor, prevented the antagonism by dexamethasone of responses to the mu opioid agonists. 5. Our data indicate that in the rodent brain there is an important functional interaction between the corticosteroid and the opioid systems at least at the mu receptor level, while delta and kappa receptors are modulated in different ways.
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PMID:Dexamethasone-induced selective inhibition of the central mu opioid receptor: functional in vivo and in vitro evidence in rodents. 788 99

Extraction of multiple third molar teeth can cause significant postoperative pain, swelling and trismus, which may result in delayed hospital discharge. We have examined the effect of a single prophylactic dose of oral dexamethasone 8 mg on these complications, in a randomised double-blind study of 50 adult patients. The number of extractions performed and the operative approach were standardised. Dexamethasone resulted in a significant reduction in pain 4 h postoperatively, and eliminated the need for opioid analgesia in the postoperative period. The incidence of severe swelling was also reduced significantly, but there was no effect on trismus. Postoperative nausea and vomiting were significantly lower in the dexamethasone group. We conclude that the use of prophylactic oral dexamethasone is useful in reducing postoperative analgesia requirements in this group of patients, and may facilitate surgery performed on a day case basis.
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PMID:Dexamethasone reduces pain and swelling following extraction of third molar teeth. 825 Jan 91


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