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. Male Sprague-Dawley rats were fitted with intrathecal (i.t.) and intracerebroventricular (i.c.v.) catheters. Fentanyl was injected either i.t. or i.c.v., and the antinociceptive efficacy of fentanyl was evaluated using the tail-flick analgesiometric assay. 2. Fentanyl dose-dependently elevated tail-flick latency (TFL) following i.c.v. or i.t. administration. The antinociceptive effects of fentanyl were reversed by naltrexone. 3. Experiments were also designed to evaluate the effects of serotonin and alpha-adrenoceptor antagonists on i.t. or i.c.v. fentanyl-induced elevations in TFL. 4. Phentolamine administered i.t. reversed both the spinal and supraspinal antinociceptive effects of fentanyl, whereas i.t. methysergide did not significantly alter the i.t. or i.c.v. effects of the mu agonist. 5. These data suggest that fentanyl-induced antinociception does not rely on local serotonergic neuronal activation. Due to the highly lipophilic nature of fentanyl, it is possible that the noradrenergic component contributing to spinal fentanyl-induced analgesia is supraspinally-mediated.
Gen Pharmacol 1992 Nov
PMID:The noradrenergic component contributing to spinal fentanyl-induced antinociception is supraspinally mediated. 133 47

1. General anaesthesia is a state of analgesia and impaired cognitive function that results from the depressant effects of anaesthetics. 2. Graded increases in anaesthetic concentration cause a progressive impairment of cognitive function, the extremes of which are commonly described as "light" and "deep" anaesthesia. 3. Surgical stimulation produces activation in the EEG and may arouse a patient from a deeper to a lighter state of cognitive function. 4. It may be very difficult, particularly in patients with neuromuscular blockade, to identify a change in state which results in conscious awareness. 5. A range of methods has been used for evaluating depth of anaesthesia. 6. The evidence reviewed in this paper suggests that the median frequency in the EEG and the auditory evoked potential appear to be the best techniques for monitoring the graded effects of anaesthetics on the brain. 7. The median frequency, which is 10 Hz in conscious subjects, should be kept below 5 Hz during anaesthesia to ensure that there is no response to verbal command. 8. The auditory evoked potential measures the resulting effects of anaesthetic depression and surgical stimulation which is "depth of anaesthesia". 9. However it is not yet certain whether a particular feature e.g. Nb latency, or a collection of features between 20 and 80 msec gives the most reliable index of conscious awareness.
Gen Pharmacol 1992 Nov
PMID:Evaluation of the actions of general anaesthetics in the human brain. 148 30

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.
Gen Pharmacol 1991
PMID:The interaction of peripherally and centrally administered dexamethasone and RU 38486 on morphine analgesia in mice. 176 Nov 97

1. Serotonin (5-HT) and selective 5-HT receptor agonists were administered intrathecally (i.t.) in rats, and the antinociceptive efficacy of these agents was assessed on the tail-flick and hot plate tests. 2. The 5-HT receptor agonists examined in this study included the 5-HT1A agonist 8-hydroxy-N,N-dipropyl-2-aminotetralin (8-OH-DPAT), the 5-HT1B agonist m-trifluoromethylphenylpiperazine (TFMPP), the 5-HT2 agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) and the 5-HT3 agonist phenylbiguanide (PBG). 3. None of these agents produced significant elevations in tail-flick latency (TFL) at doses which produced elevations in hot plate latency (HPL). 4. In contrast, the i.t. dose of 5-HT which elevated TFL also produced analgesia on the hot plate test. 5. Serotonin-induced elevations in TFL were reversed by pindolol, ritanserin and ICS 205-930, suggesting that 5-HT interacts with more than one 5-HT site in the spinal cord to produce analgesia on the tail-flick test. 6. The finding that ritanserin reversed 5-HT-induced elevations in HPL suggests that the 5-HT2 site is primarily responsible for mediating the spinal antinociceptive effects of 5-HT on the hot plate test.
Gen Pharmacol 1991
PMID:Analgesic effects of serotonin and receptor-selective serotonin agonists in the rat spinal cord. 182 46

1. Four different strains of mice were used to study the influence of psychogenetics in opiate tolerance and abstinence. 2. The CD1 strain seemed to be more sensitive to naloxone administration after four days of morphine implantation, because administration of the antagonist induces a number of jumps in the withdrawal phase higher than in the case of the DBA or C3H strains. 3. DBA and C3H mice elicit analgesia before the CD1 strain, whereas the C3H mice lose body weight at a faster rate than the other strains. 4. C57 bl mice died after morphine implantation (100%). 5. These findings are discussed in relation with neurochemical and receptor variations.
Gen Pharmacol 1991
PMID:Influence of psychogenetics in opiate tolerance and abstinence in mice. 193 7

1. Diltiazem, verapamil and nifedipine produced a dose-dependent analgesic response in mice. 2. A fixed oral dose of acetylsalicylic acid increased this analgesic response. 3. Analgesia was maintained when mice were treated chronically with calcium channel blockers alone or when combined with aspirin.
Gen Pharmacol 1991
PMID:Effect of diltiazem, nifedipine and verapamil on the antinociceptive action of acetylsalicylic acid in mice. 205 Feb 80

1. The analgesic effects of diltiazem and verapamil, both per se and together with morphine, were studied using subcutaneous (s.c.) and intracerebroventricular (i.c.v.) administrations, in the hot-plate test in mice. 2. The i.c.v. injection of verapamil (15-120 micrograms/mouse) and diltiazem (60-120 micrograms/mouse) induced dose-dependent analgesic effects. 3. The i.c.v. administration of verapamil (30-120 micrograms/mouse) and diltiazem (60-120 micrograms/mouse) significantly enhanced, in a dose-dependent way, the analgesic effects of morphine and produced a parallel displacement to the left of the morphine log dose-response line. 4. When these calcium channel blockers were administered subcutaneously at doses of 40 and 80 mg/kg, they exerted no analgesic actions, but dose-dependently potentiated the analgesic effects of morphine, producing a parallel shift to the left of the morphine log dose-response line. 5. These results suggest that inhibition of calcium entry through calcium channels induced by verapamil and diltiazem may play a role in analgesia development.
Gen Pharmacol 1990
PMID:Analgesic effects of diltiazem and verapamil after central and peripheral administration in the hot-plate test. 227 85

1. The analogs of adenosine D- and L-phenylisopropyladenosine (D- and L-PIA) and chloroadenosine (CADO) induced analgesia in mice (hot-plate test). 2. The antinociceptive effects of the three adenosine agonists were antagonized by caffeine but were unaffected by naloxone. 3. Morphine-induced antinociception was increased by pretreatment with adenosine agonists. 4. Whereas CADO significantly attenuated the induction of morphine tolerance, D- and L-PIA did not affect the process.
Gen Pharmacol 1990
PMID:Effects of some adenosine analogs on morphine-induced analgesia and tolerance. 227 94

1. The effects of intraperitoneal administration of a standard extract of Panax ginseng alone and in combination with morphine were determined in male Sprague-Dawley rats. 2. Ginseng extract at 200 mg/kg produced analgesia and hypothermia. These effects of ginseng were not reversed by naltrexone. 3. A dose of morphine (8 mg/kg) produced analgesia and hyperthermia. The analgesic response to morphine was antagonized by 25 and 50 mg/kg doses of ginseng but not by 12.5, 100 and 200 mg/kg doses. 4. Morphine-induced hyperthermia was antagonized by 12.5-200 mg/kg doses of ginseng. 5. Administration of morphine (50 mg/kg) produced cataleptic effect which was antagonized by 25 mg/kg of ginseng. 6. The results suggest that ginseng extract at high doses produces analgesia and hypothermia in the rat by a non-opiate mechanism, and antagonizes the acute pharmacological effects of morphine.
Gen Pharmacol 1990
PMID:Antagonism of the acute pharmacological actions of morphine by panax ginseng extract. 227 87

We tested the hypothesis that exposure to a stimulus resembling the original traumatic event would induce naloxone-reversible analgesia in patients with posttraumatic stress disorder (PTSD). Eight medication-free Vietnam veterans with PTSD and eight veterans without PTSD, matched for age and combat severity, viewed a 15-minute videotape of dramatized combat under naloxone hydrochloride and placebo conditions in a randomized double-blind crossover design. In the placebo condition, the subjects with PTSD showed a 30% decrease in reported pain intensity ratings of standardized heat stimuli after the combat videotape. No decrease in pain ratings occurred in the subjects with PTSD in the naloxone condition. The subjects without PTSD did not show a decrease in pain ratings in either condition. The results are consistent with the induction of opioid-mediated stress-induced analgesia in the patients with PTSD.
Arch Gen Psychiatry 1990 Jun
PMID:Naloxone-reversible analgesic response to combat-related stimuli in posttraumatic stress disorder. A pilot study. 235 Feb 6


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