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)

Sixty-six patients undergoing total knee arthroplasty were offered epidural morphine as a method of postoperative analgesia. Of the 66 patients, 50 completed the minimum protocol of 3 days in a special epidural monitoring unit and were thus available for study. In this study group, 86% stated that they obtained 75-100% relief of pain with each epidural injection. Greater than 90% of the patients rated the overall experience with epidural analgesia as excellent or good. Ninety percent stated that they would choose epidural morphine analgesia again if given the choice. Nausea and vomiting were the most common adverse effects, occurring in 34%. One patient experienced respiratory depression, which was reversed with Narcan. The most frequent complaint related to the procedure itself was the use of an apnea monitor; 18% of the patients considered this monitoring device intolerable. The progress of total knee arthroplasties in the epidural unit was monitored by range of motion achieved. At 72 hours the average motion was 10 degrees-87 degrees and at the end of the hospital stay was 6 degrees-98 degrees. The total hospital bill for epidural morphine analgesic patients was $469 more than for a conventional arthroplasty patient, though the mean duration of hospital stay was 1.7 days less for the epidural morphine patients. Epidural morphine provided excellent but inconsistent postoperative pain relief. When relief was present, aggressive in-house rehabilitation could be instituted, and a shorter overall hospital stay was achieved when compared with conventional analgesia. Nonetheless, the related adverse effects and inconsistent pain relief on many patients may preclude the use of epidural morphine as a single postoperative analgesic agent.
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PMID:The use of epidural morphine in patients undergoing total knee arthroplasty. 250 54

Rats were randomly divided into 4 groups: Control, Electro-acupuncture (EA), Naloxone and Naloxone plus EA. The content of noradrenaline (NA) and dopamine (DA) in brain stem, diencephalon and telencephalon were determined by spectrofluorometry. It was found that the pain threshold increased and the NA content in the telencephalon decreased and the DA level in the brain stem increased markedly after EA. Naloxone injection partially decreased the analgesic effect of EA and abolished the EA-induced elevation of DA in the brain stem and attenuated the NA level in the diencephalon after EA. These results suggest that morphine receptor may play an important role in EA analgesia and this may be partially carried out through the brain catecholamine system.
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PMID:[Effects of intraperitoneal injection of naloxone on the analgesic effect and the changes of brain catecholamine contents induced by electroacupuncture in rats]. 251 24

The influence of YM-14673 (N alpha-[[(S)-4-oxo-2-azetidinyl]-carbonyl]-L-histidyl-L-prolinamide dihydrate), a new thyrotropin releasing hormone (TRH) analogue, on morphine-induced hypothermia, development of cerebral ischemia and analgesia was investigated in rodents. YM-14673, in doses not affecting the normal rectal temperature, antagonized morphine-induced hypothermia in mice. Morphine-induced hypothermia was also antagonized by administration of TRH, in doses increasing normal rectal temperature. Morphine increased the appearance rate of convulsions in rats subjected to bilateral occlusion of the carotid artery. YM-14673, unlike TRH, reduced the appearance rate of convulsions increased by morphine in the ischemic rats. Morphine-induced analgesia measured by the hot plate method was not affected by both YM-14673 and TRH. Naloxone antagonized the effect of morphine in the 3 models. These results suggest that YM-14673 possesses physiological opioid antagonistic properties.
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PMID:Effects of YM-14673, a new TRH analogue, on responses to morphine in rodents. 251 20

Effects of yohimbine, methysergide and naloxone given intrathecally (i.t.) and naloxone given intracerebroventricularly (i.c.v.) on inhibition of the tail-flick and hot-plate response induced by beta-endorphin and morphine given i.c.v. were studied in male ICR mice. Yohimbine (1.5 and 15 micrograms) and methysergide (1.5 and 15 micrograms) injected i.t. antagonized inhibition of the tail-flick response induced by morphine but not beta-endorphin administered i.c.v. On the other hand, naloxone (20 ng) injected i.t. antagonized inhibition of the tail-flick response induced by i.c.v. administered beta-endorphin but not morphine. Yohimbine and methysergide given i.t. did not antagonize inhibition of the hot-plate response induced by morphine nor did naloxone given i.t. antagonized i.c.v. beta-endorphin-induced inhibition of the hot-plate response. Naloxone given i.c.v. was more effective in antagonizing morphine-induced inhibition of the tail-flick and hot-plate response than inhibition induced by beta-endorphin given i.c.v. Naloxone at doses (0.1 and 1 microgram) which effectively reversed inhibition of the tail-flick response to i.c.v. morphine was not effective in reversing the i.c.v. beta-endorphin-induced inhibition of the tail-flick response. Our results indicate that beta-endorphin and morphine produce analgesia by stimulating separate types of opioid receptors, epsilon- for for beta-endorphin and mu- for morphine, and activate separate descending pain modulatory control systems. The supraspinal epsilon system stimulated by beta-endorphin is mediated by activation of spinal opioid receptors whereas the supraspinal mu system stimulated by morphine is mediated by activation of spinal alpha 2-adrenoceptors and serotonin receptors for the production of analgesia.
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PMID:Differential mechanisms mediating beta-endorphin- and morphine-induced analgesia in mice. 253 Oct 93

In a recent study [30] it was reported that naloxone, at doses normally employed for opioid antagonism, produced a dose-dependent analgesia in BALB/c mice in the formalin test. We report here that another opioid antagonists, naltrexone, also produces analgesia under these conditions. Female BALB/c mice were injected subcutaneously with naltrexone (0.01-1.0 mg/kg) or saline alone and tested for analgesia using the formalin test. Naltrexone produced a statistically significant dose-dependent analgesia, with an ED50 of 0.05 mg/kg and almost total analgesia at doses of 0.1 mg/kg or greater. To determine the relationship between naloxone analgesia and better documented forms of opioid analgesia, BALB/c mice were injected with naloxone or saline following the administration of a pre-determined ED50 for morphine and tested for analgesia using the tail-flick and formalin tests. Naloxone antagonized morphine analgesia in the tail-flick test at both doses used (0.3 and 10 mg/kg). In the formalin test, however, naloxone attenuated morphine analgesia at the lower doses (0.1 and 0.3 mg/kg) and potentiated morphine analgesia at the highest dose (10 mg/kg). The implications of this finding are discussed.
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PMID:Analgesia produced by normal doses of opioid antagonists alone and in combination with morphine. 253 85

Mice of the Swiss-Webster strain obtained from two suppliers (Taconic, Charles River) were found to differ in their sensitivity to morphine. Mice from Taconic were approximately two-fold more sensitive to the analgesic and lethal effects of morphine compared to the Charles River mice. In a third strain, C3H/HEN, morphine was found to be more than 2.5 times more potent in producing analgesia than in the Charles River mice. Binding studies showed that the Taconic mice and C3H/HEN mice had approximately 40% and 60%, respectively, more specific [3H]naloxone binding sites in brain than did the less sensitive Charles River mice. When treated with chronic naltrexone for 8 days the analgesic potency of morphine was increased by approximately 90% for both Swiss-Webster mice and by 20% for the C3H/HENs. [3H]Naloxone binding was increased by 45-50% in the Swiss-Webster strains, but by only 33% in C3H/HEN mice. These data indicate that receptor upregulation is directly related to increases in morphine potency. Further, these findings suggest that initial sensitivity to morphine can determine the degree of functional supersensitivity and relative receptor upregulation produced by chronic opioid antagonist treatment.
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PMID:Opioid receptor upregulation and supersensitivity in mice: effect of morphine sensitivity. 254 6

NalBzoH (6-desoxy-6-benzoylhydrazido-N-allyl-14-hydroxydihydronomorphin one) is a novel opiate with potent actions at both mu and kappa receptors. Analgesic studies in mice examining increasing doses of NalBzoH with a fixed dose of morphine revealed a biphasic curve. NalBzoH at doses as low as 1 microgram/kg partially antagonized morphine analgesia. Higher NalBzoH doses continued to inhibit morphine analgesia in a dose-dependent manner, with the 1-mg/kg dose antagonizing completely morphine analgesia. As the NalBzoH dose increased beyond 1 mg/kg analgesia returned. NalBzoH also prduced a similar analgesic response when administered alone in mice and also was active in rats. NalBzoH had excellent p.o. activity, with an analgesic potency in mice equivalent to s.c. administration. Naloxone reversed NalBzoH analgesia far less effectively than morphine analgesia. In contrast, Win44,441 antagonized both morphine and NalBzoH analgesia with a similar potency, consistent with a kappa mechanism for NalBzoH analgesia. Repeated administration of NalBzoH resulted in tolerance. There was no analgesic cross-tolerance between NalBzoH and either morphine or the kappa 1-selective agent U50,488H, implying a selective kappa 3 mechanism of analgesia. In addition to blocking morphine analgesia, low doses of NalBzoH also partially reversed the inhibition of gastrointestinal transit in mice produced by morphine, antagonized completely morphine lethality and precipitated withdrawal in morphine-dependent mice, confirming its antagonist activity in mu receptors. The duration of NalBzoH's kappa and mu actions differed dramatically. In mice, analgesia typically lasted less than 2 hr whereas the same NalBzoH dose antagonized completely morphine analgesia, a mu action, for 16 hr. Full sensitivity to morphine did not return for 32 hr.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pharmacological actions of a novel mixed opiate agonist/antagonist: naloxone benzoylhydrazone. 255 21

Sulfated cholecystokinin octapeptide (CCK-8; Asp-Tyr-SO3H-Met-Gly-Trp-Met-Asp-Phe-NH2) produced analgesia in mice when administered i.c.v. and tested in the acetic acid-induced writhing assay. The ED50 was found to be 0.03 nmol/mouse which was about 3, 24 and 714 times more potent than morphine. [D-Pen2,D-Pen5]enkephalin and U50,488H [trans-(+/-)-3,4-dichloro-N-methyl-N-[2-(1-pyrolidinyl)cyclohexyl] benzeneacetamidel], respectively. When administered i.t., CCK-8 produced partial analgesia of up to 22 to 23% at low doses ranging from 15 to 60 ng/mouse and hyperalgesia at doses over 120 ng/mouse. Naloxone, an opioid antagonist, inhibited the analgesia induced by CCK-8 (i.c.v. and i.t.) but potentiated hyperalgesia induced by CCK-8 (i.t.). Apparent pA2 value for CCK-8 (i.c.v.) against naloxone (s.c.) was 5.88 which was significantly different from those for morphine-naloxone and U50,488H-naloxone but was not significantly different from that for [D-Pen2,D-Pen5]enkephalin-naloxone. Studies using highly selective opioid antagonists showed that CCK-8-induced analgesia was significantly antagonized by the delta receptor antagonist, ICI154,129 [(Allyl)2-Tyr-gly-gly-psi-(CH2S)-Phe-Leu] but not by beta-funaltrexamine, a highly selective mu receptor antagonist or nor-binaltorphimine, a highly selective kappa receptor antagonist. Opioid receptor binding study using [3H]-[D-Ala2,D-Leu5]enkephalin (+unlabeled [D-Ala2,MePhe4,Gly-ol5]enkephalin) in mouse brain membrane preparations revealed that there were no changes in the maximum binding or Kd of delta opioid binding sites in the presence of CCK-8 (1 microM) in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Indirect involvement of delta opioid receptors in cholecystokinin octapeptide-induced analgesia in mice. 255 28

Microinjection of morphine sulfate into dorsal raphe, ventrolateral central gray and dorsolateral central gray inhibits spinal nociceptive reflexes. The effects of the blockade of spinal opioid, adrenergic, and serotonergic receptors by intrathecal injection of naloxone, yohimbine and methysergide, respectively, on inhibition of the tail-flick response induced by morphine microinjected into dorsal raphe, ventrolateral central gray and dorsolateral central gray were studied. Naloxone (20 micrograms) given intrathecally effectively antagonized inhibition of the tail-flick response induced by morphine (4 micrograms) given into dorsal raphe and ventrolateral central gray, but not dorsolateral central gray. On the other hand, intrathecal injection of yohimbine (30 micrograms) antagonized inhibition of the tail-flick response induced by morphine given into ventrolateral central gray and dorsolateral central gray, but not dorsal raphe. Intrathecal injection of prazosin (30 micrograms) did not antagonize inhibition of the tail-flick response induced by morphine given into dorsal raphe or lateral central gray. Intrathecal injection of methysergide (30 micrograms) only partially antagonized inhibition of the tail-flick response induced by morphine given into dorsal raphe, but not ventrolateral central gray and dorsolateral central gray. It is concluded that the analgesia induced by morphine injected into dorsal raphe is mediated by spinal opioid receptors but not by spinal alpha 2-adrenergic receptors while the analgesia produced by morphine given into dorsolateral central gray is mediated by spinal alpha 2-adrenergic receptors. The analgesia induced by morphine given into ventrolateral central gray is mediated in part by both spinal alpha 2-adrenergic and opioid receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential actions of the blockade of spinal opioid, adrenergic and serotonergic receptors on the tail-flick inhibition induced by morphine microinjected into dorsal raphe and central gray in rats. 255 62

The hypothesis that genetic differences in opiate receptor concentration are involved in determining the sensitivity to some of the effects of alcohol was studied by comparing the hypothermic and analgesic effects of ethanol in four strains of mice that can be divided into three groups on the basis of their brain opiate receptor concentration: high (CXBH), low (CXBK) and intermediate (C57BL/6By and BALB/cBy). In the first experiment, animals within each strain were injected with either saline or 1.5 g/kg ethanol and their pain sensitivity was assessed 20 min later by the hot-plate test. The same procedure was repeated 10 days later with a higher dose of ethanol (2.5 g/kg). The lower dose produced analgesia only in CXBH mice, whereas the higher dose produced analgesia in CXBH, C57BL/6By and BALB/cBy mice, but had no effect in CXBK mice. In the second experiment, animals within each strain were injected with either saline or naloxone, followed 20 min later by an injection of 3.5 g/kg ethanol. CXBH mice were significantly more hypothermic and CXBK mice were significantly less hypothermic than all other strains. Naloxone attenuated ethanol's hypothermic effect in all strains except CXBK. These results suggest that the hypothermic and analgesic effects of ethanol are at least partly mediated by opiate receptors and are correlated with genetic differences in opiate receptor concentration.
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PMID:Genetic differences in opiate receptor concentration and sensitivity to ethanol's effects. 255 15


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