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)

Epidural analgesia inhibits several metabolic effects of trauma. Some of these effects are generated by the endogenous fever mediator interleukin-1. Postoperative fever was therefore studied in 52 patients, 25 of whom had had epidural analgesia and 27 general anaesthesia. Transvesical prostatectomy was used as standard surgical trauma. Most of the patients had postoperative temperature rise exceeding 0.5 degree C, but the rise was not influenced by epidural analgesia. These data suggest that the release of endogenous fever mediator is not under control of afferent pathways from the region of trauma. The findings are also consistent with regulation of interleukin-1 release which is independent of adrenal stimulation, cyclic AMP or beta-endorphin, as epidural analgesia prevents postoperative increase of these hormones.
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PMID:Influence of neural pathways on the pyrexial response to surgical trauma. 387 48

The effects of neurogenic block on plasma concentrations of adrenaline, noradrenaline and cyclic AMP were studied. Eighteen patients were subjected to surgery of moderate or minor extent under enflurance anesthesia with or without epidural analgesia. The results show that adrenaline secretion during surgical stress is a response to neurogenic stimuli, since the increase found in patients subjected to hysterectomy under general anesthesia is blocked by the addition of epidural analgesia. Furthermore, plasma adrenaline after neurogenic block is comparable with adrenaline levels during minor surgical stress. The plasma noradrenaline concentration does not correlate with the extent of trauma. In contrast to adrenaline levels, noradrenaline concentrations varied insignificantly during and after surgery. However, the addition of epidural block induced a postoperative increase in noradrenaline apparently unrelated to changes in heart rate or blood pressure. Simultaneous measurements of the catecholamines and cyclic AMP indicate that adrenaline is of minor importance for plasma cyclic AMP in resting patients, whereas the increase in cyclic AMP elicited by surgery reflects adrenaline-stimulated beta-adrenergic activity.
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PMID:Influence of epidural analgesia on the catecholamine and cyclic AMP responses to surgery. 624 5

Pain sensitivity and analgesia induced by the stimulation of the ventral tegmentum (VT) were studied in 72 male rats of two lines, LC2-Hi and LC2-Lo, genetically selected for high and low rates of lateral hypothalamic self-stimulation, respectively. LC2-Lo rats were more sensitive to acute peripheral pain and developed a stronger analgesia than their LC2-Hi counterparts. In order to assess the pharmacological substrate of ventral tegmental stimulation-induced analgesia (VT-SIA), the effects of amphetamine (AMP, 21 animals), naloxone (NX, 24 animals) and parachlorophenylalanine (PCPA, 27 animals) injections were studied. VT-SIA was found to be clearly decreased by PCPA, slightly decreased by AMP and not significantly affected by NX. Ventral tegmental self-stimulation ( VTSS ) was increased by PCPA treatment. The comparison of VTSS and VT-SIA did not reveal any correlation between both phenomena. These data suggest that VT-SIA may be mediated by serotonin while catecholamines may have a modulatory role in this analgesia and that VTSS and VT-SIA seem to be governed by different neuronal systems.
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PMID:Ventral tegmental analgesia in two strains of rats: effects of amphetamine, naloxone and parachlorophenylalanine. 632 24

In C57BL/6 mice caffeine antagonized morphine-induced hyperactivity. This effect was most evident when caffeine was used in doses that slightly increased locomotor activity. Given at the same dose caffeine did not affect morphine-induced analgesia. Two possibilities of explanation of this effect are discussed: action of caffeine on dopaminergic mechanisms responsible for morphine-induced running fit through its effect on cyclic AMP level, and a direct action of caffeine on delta opiate receptors involved in the stimulatory effect of morphine.
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PMID:Caffeine interferes with morphine-induced hyperactivity but not analgesia. 667 94

1. The effects of acute and chronic lithium (Li+) treatments on the antinociception caused by morphine were studied in mice using the tail-flick test. 2. Subcutaneous injection of morphine (10 mg/kg) caused significant antinociception. 3. Acute Li+ administration (0.05, 0.1, 0.3, 1, 5 and 10 mg/kg, i.p.) alone had no significant antinociceptive effect but changed morphine analgesia; low doses of Li+ (0.1, 0.3 and 1 mg/kg) were found to decrease the antinociception induced by morphine whereas higher doses of the drug (10 mg/kg) potentiated this effect. 4. The 6 day administration of Li+ with a serum level of 0.528 mM decreased the antinociceptive effect of morphine. 5. The effect of Li+ on morphine-induced analgesia persisted for 96 hr in spite of the fact that Li+ drinking was discontinued (the serum Li+ level decreased from 0.528 to 0.022 mM). 6. It has been reported that Li+ might change both the binding of opioids to their receptors and biosynthesis or release of endogenous opioids. There is also a considerable body of evidence which indicates that both Li+ and morphine affect phosphoinositide turnover, intracellular calcium content and cyclic AMP level. The interaction of two drugs may conceivably take place through these systems. 7. These data suggest that the biological effects of Li+ may exist at very much lower serum Li+ levels than the commonly accepted therapeutic range.
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PMID:The effect of lithium on morphine-induced analgesia in mice. 772 Oct 39

The effects of pertussis toxin, forskolin, and cAMP analogues on the antinociceptive action of nicotine were examined to investigate the possible involvement of adenylate cyclase and G-proteins in nicotine's antinociceptive effect. Intrathecal injection of pertussis toxin (0.25 and 0.50 micrograms) in mice inhibited nicotine-induced antinociception in the tail-flick test. The effect of the toxin was dose and time dependent. Forskolin, a potent adenylate cyclase activator, and 8-(-4-chlorophenylthio) adenosine-3':5' monophosphate, cyclic (8-CPT-cAMP), a cAMP analogue, inhibited the antinociceptive effects of nicotine in a dose-dependent manner. EGTA reversal of 8-CPT-cAMP's inhibitory effects suggests that calcium may to be involved. These data implicate the possible involvement of a G-protein and a second messenger system (activation of a cAMP-dependent protein kinase and increase in cyclic AMP levels) in nicotine-induced analgesia in mice.
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PMID:Nicotine-induced antinociception in mice: role of G-proteins and adenylate cyclase. 802 3

Twenty patients undergoing abdominal surgery under general anaesthesia were studied to determine whether beta 2-adrenergic receptor sensitivity and adrenaline-induced hypokalaemia are related to preceding adrenergic stress. Half of the patients were given epidural analgesia with bupivacaine-adrenaline before starting surgery and then a booster dose after 60 min of surgery. The others were given only the epidural dose of bupivacaine-adrenaline at 60 min. Despite marked increases in the plasma adrenaline concentration after the intra-operative epidural dose, there was no decrease in the serum potassium concentration in either group. In the patients who received only the 60 min dose, the plasma adrenaline concentrations increased more, but the plasma level of cyclic AMP (a marker for beta 2-stimulation) increased similarly, which suggests that beta 2-adrenoceptor responsiveness was somewhat reduced. After the intraoperative bupivacaine-adrenaline, the T wave amplitude decreased, but neither U waves nor tachycardia developed. In conclusion, adrenergic stimulation during surgery does not decrease the serum potassium concentration, regardless of whether the surgical stress response has been modified by epidural analgesia. This lack of a hypokalaemic effect might be partly due to reduced responsiveness of beta 2-adrenoceptors to adrenaline.
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PMID:Adrenaline, cyclic AMP and potassium during general anaesthesia with and without epidural analgesia. 854 57

We analyzed the pharmacological characteristics of (-)-3-acetyl-6 beta-acetylthio-N-cyclopropylmethyl-normorphine (KT-90) using Chinese hamster ovary (CHO) cells expressing cloned rat mu-, delta- and kappa-opioid receptors. KT-90 displaced the specific binding of the following radiolabeled ligands selective to the mu-, delta- and kappa-opioid receptors, [3H][D-Ala2,MePhe4,Gly(ol)5]enkephalin (DAMGO), [3H][D-Pen2,D-Pen5]enkephalin (DPDPE), [3H] (+)-(5 alpha, 7 alpha, 8 beta)-N-methyl-N-[7-(1-pyrrolidinyl) l-oxaspiro-(4,5)dec-8-yl]benzeneacetamide (U69,593), with Ki values of 3.3 +/- 0.7, 22.8 +/- 1.5 and 1.9 +/- 0.3 nM, respectively In CHO cells expressing the mu-, delta- and kappa-opioid receptors, KT-90 inhibited forskolin (10 microM)-induced cyclic AMP accumulation in a concentration-dependent manner with IC50 values of 2337 +/- 750, 17.3 +/- 4.6 and 2.0 +/- 0.1 nM, respectively. The maximal inhibitory effects of KT-90 in the cells expressing mu-, delta- and kappa-opioid receptors were significantly lower than those of the type-selective agonists DAMGO, DPDPE and U69,593, respectively. These results indicated that KT-90 acts as a partial agonist on mu-, delta- and kappa-opioid receptors. KT-90 (10 and 100 nM), when added with morphine, produced a rightward shift of the concentration-response curve of morphine to inhibit the cyclic AMP accumulation in CHO cells expressing mu-, but not delta- or kappa-, opioid receptors. This finding is consistent with the findings that lower doses of KT-90 antagonize morphine analgesia in vivo.
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PMID:Pharmacological characterization of KT-90 using cloned mu-, delta- and kappa-opioid receptors. 889 18

It was proposed that the repetitive rapid-rate transcranial magnetic stimulation (TMS) induces the functional and structural changes analogous to those which are evoked during the electroconvulsive treatment. Presently, we compared the effects of 8 daily treatments with TMS (t = 5 min, B = 0.1 T, trise = 200 microseconds, f = 50 Hz) and electroconvulsive shock (ECS) (t = 0.5 s, I = 150 mA, f = 50 Hz) on the behavior of rats in the forced swimming test (24 h after the last treatment), the exploratory activity test (0-10 min), the basal locomotor activity test (11-30 min), and the tail flick test (2 h after the last treatment). We also tested (24 h after the treatment) the reactivity of the cyclic AMP generating system in cerebral cortical slices. Statistical significance of the results was estimated by ANOVA and t-Student test. The immobility time in the forced swimming test was shortened after TMS and ECS to 86 and 75% of control values, respectively (p < 0.05 and p < 0.01). Both ECS and TMS depressed the basal locomotor activity (by 60 and 80%, resp.), and ECS, but not TMS, diminished also the exploratory activity by 70% (p < 0.01) only ECS induces analgesia, prolonging tail-flick latency by 90% (p < 0.01). ECS diminished the accumulation of the noradrenaline-stimulated cyclic AMP in the cortex slices (by 35%; p < 0.05). The effect after TMS was similar but statistically not significant (87% of control values). The data suggest that TMS produces in rats some responses that are regarded as predictive for the antidepressant activity, similar to those produced by ECS, but less side effects.
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PMID:[Behavioral and biochemical effects of magnetic brain stimulation and electroshock in rats]. 897 60

In this study, mice received a single intracerebroventricular (i.c.v. ) injection of an antisense oligodeoxynucleotide (ODN) directed towards the mRNA of Gialpha2. Controls received a saline or a nonsense ODN injection. The subsequent effects on protein levels and mRNA of Gialpha2 were determined in mouse striatum, as well as, the effect on opioid ([d-Ala2, d-Leu5]-enkephalin; DADLE) inhibition of cyclic AMP (cAMP) formation in striatum and morphine analgesic potency. At 48 h after treatment, maximal inhibition (Emax) of cAMP formation was significantly reduced for the antisense group compared to controls. Antisense ODN treatment only changed the Emax and did not significantly alter the IC50s of the dose-effect curves for inhibition of cAMP formation. Antisense ODN, but not nonsense ODN, significantly reduced morphine's analgesic potency by >2-fold, 48 h following treatment. Using a quantitative immunoblotting procedure, antisense treatment was shown to decrease striatal Gialpha2 protein 48 h after antisense injection, while there were no changes in protein levels at 2, 12 and 24 h. In contrast, no changes in Gialpha2 mRNA in mouse striatum were noted at any time after antisense treatment. Taken together, these data suggest that Gialpha2 mediates opioid-induced analgesia and opioid inhibition of cAMP production in the mouse. These data also suggest that antisense reduces target protein by a mechanism independent of changes in mRNA abundance.
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PMID:The effects of antisense to Gialpha2 on opioid agonist potency and Gialpha2 protein and mRNA abundance in the mouse. 972 12


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