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)

Tolerance to various effects of morphine in the rat can be quantified by means of a shift of semi-logarithmic dose-response curves. Tolerance to analgesia (hot plate, acetic acid writhing), catalepsy, and the tilted plane develops in a closely similar manner. Also, the stimulating effects of about 1 mg/kg morphine-HC1 tested in an open-field procedure are somewhat less pronounced in chronically treated rats than in naive ones. There is no correlation between tolerance development and the acute ED50 of different tests.
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PMID:The development of tolerance to morphine in the rat. 41 15

1. Tolerance to morphine-induced analgesia (hot plate and acetic acid whrithing test), hypothermia and lethality can be quantified in mice by measuring the degree of parallel shifts of semilog. dose-response relationships induced by repeated opioid administration. 2. A similar procedure can be used for the quantification of naloxone-induced withdrawal as an indicator of dependence. 3. The intensity of tolerance development with respect to time of administration and dosage of morphine varies with the test procedure. It is closely parallel, however, in both analgesic tests during acquisition of tolerance. 4. Log-log-linear relationships exist between tolerance in analgesic tests and physical dependence as determined by naloxone-induced withdrawal. 5. The minimum tolerance-inducing dose of morphine in different tests could not be correlated to the ED50's in these tests. 6. Chronic opiate treatment leads to a decrease or an increase in motility response to morphine, depending on the time that has elapsed after the last morphine administration.
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PMID:Quantitative assessment of tolerance to and dependence on morphine in mice. 55 28

Effects of beta-(p-chlorophenyl)-GABA (baclofen), a muscle relaxant, on the response of mice and rats to various noxious stimuli were studied. In mice, 5 approximately 10 mg/kg i.p. of baclofen delayed the response time to tail-pinch and hot-plate stimuli but the relaxation was also apparent with this dose range. Mephenesin also delayed the response time to tail-pinch stimuli with the dose producing muscle relaxation. Baclofen, 3 mg/kg i.p., while producing no muscle relaxation, suppressed the acetic acid-induced writhing. The same effect, suppression of writhing and no muscle relaxation, was achieved with 50 mg/kg i.p. of mephenesin. In rats, baclofen (5 approximately 10 mg/kg i.p.) increased the response threshold in Randall-Selitto method and suppressed the bradykinin-induced symptoms, however, muscle relaxation was also produced with these same doses. Increase in response threshold in Randall-Selitto method was achieved with the dose of mephenesin producing muscle relaxation. The time courses of the depression of response to noxious stimuli and the muscle relaxation induced by baclofen and mephenesin were consistent in mice and rats. A small dose (3 mg/kg i.p. in mice, 2 mg/kg/h s.c. in rats) of baclofen reduced the antinociceptive effect of morphine but a larger dose (5 mg/kg i.p. in mice, 7 mg/kg/h s.c. in rats) of baclofen increased or did not alter the effect of morphine. It seems likely that the antinociceptive effect of baclofen may be nonspecific to analgesia.
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PMID:[Effects of beta-(p-chlorophenyl)-GABA (baclofen) on response to noxious stimuli (author's transl)]. 59 82

1. The antinociceptive effect of prostaglandins E1, E2 and F2alpha was studied in albino rats. Though all three prostaglandins produced similar degrees of sedation, only prostaglandin E1 (PGE1) produced a dose-related antinociceptive activity. 2. The antinociceptive activities of equi-analgesic doses of morphine (7.5. mg/kg, i.p.) and PGE1 (2.0 mg/kg, i.p.) were inhibited to almost similar extents after pretreatment with drugs known to reduce central turnover of serotonin receptors, namely reserpine, fenclonine (p-chlorophenylalanine), methysergide and 5,6-dihydroxytryptamine. 3. Prostaglandin F2alpha (2.0 mg/kg, i.p.) significantly inhibited the antinociceptive effects of both morphine and PGE1. 4. The prostaglandin synthesis inhibitors, indomethacin and diclofenac, significantly inhibited morphine analgesia. 5. Probenecid markedly prolonged the duration of antinociceptive effect of morphine and the duration of PGE1-induced potentiation of subanalgesic dose of morphine. 6. The results suggest that, in albino rats, PGE1-induced antinociceptive activity is serotonin mediated and that morphine analgesia is not only mediated through serotonin but also through prostaglandins (PGE1 ?) and 5-hydroxyindole acetic acid, the serotonin metabolite.
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PMID:Prostaglandins: antinociceptive effect of prostaglandin E1 in the rat. 89 Oct 40

The objective of this study was to characterize further the nature of nitrous oxide analgesia and to establish if tolerance to nitrous oxide occurs. Methods for studying the analgesic action of a gas are described. In mice, nitrous oxide is analgesic in the phenylquinone and acetic acid abdominal constriction tests. Aspirin and very high doses of alcohol are also active in these tests; however, only nitrous oxide-induced analgesia is antagonized by narcotic antagonists. These data indicate the mechanism of action of nitrous oxide analgesia differs from that of the other two drugs. Nitrous oxide produced a dose-related analgesic response in rats (ED50, 67%) as measured by the tail-flick method. Naloxone, 5 to 30 mg/kg, also antagonized nitrous oxide analgesia in rats. Lower doses of the antagonist were not effective. Tolerance developed to the effects of nitrous oxide in both rats and mice after prolonged exposure. These data lend support to the hypothesis that nitrous oxide and opiates have a significant pharmacologic resemblance and may ultimately produce similar molecular events in the brain leading to the relief of pain.
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PMID:Nitrous oxide analgesia: reversal by naloxone and development of tolerance. 92 57

A peptide material with opiate-like activity in the guinea-pig ileum was extracted from porcine pituitaries using a hot glacial acetic acid extraction method and was partially purified by gel filtration. When injected intraventricularly in rats, these purified peptides induced strong analgesia, catelepsy, respiratory depression and other opiate-like effects, which lasted for several hours.
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PMID:Porcine pituitary peptides with opiate-like activity: partial purification and effects in the rat after intraventricular injection. 103 19

The mild analgesic activities of aspirin, phenacetin and acetaminophen have been compared in the trypsin, kaolin and carrageenan hyperalgesic assays as well as in the acetic acid writhing test. The trypsin and kaolin hyperalgesic assays were designed to be unaffected by drugs with anti-inflammatory activity. Aspirin and acetaminophen were inactive in these two tests at dose levels devoid of side effects. Phenacetin was active in the trypsin and kaolin assays with oral ED50's of 114 +/- 36.2 and 107 +/- 11.5 mg/kg, respectively. Non-steroidal anti-inflammatory drugs as well as phenacetin and acetaminophen were active in the acetic acid writhing and carrageenan hyperalgesic assays. This led to evaluation of phenacetin and acetaminophen as anti-inflammatory agents. Both of these latter drugs were active in the carrageenan pleurisy and adjuvant arthritis models of inflammation. In all studies phenacetin was equipotent to or more potent than acetaminophen. The data suggest that the analgesia produced by aspirin and acetaminophen results from their anti-inflammatory activity whereas the analgesia produced by phenacetin has two components, one dependent on and one independent of anti-inflammatory activity.
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PMID:Quantitative comparison of the analgesic and anti-inflammatory activities of aspirin, phenacetin and acetaminophen in rodents. 127 45

The kappa-receptor selectivity of nor-binaltorphimine (nor-BNI), a highly selective kappa-opioid receptor antagonist in vitro, was examined in vivo by measuring the time course of the antagonistic action of nor-BNI (5 and 20 mg/kg, s.c.) against the responses to U-50488H (10 mg/kg, s.c.), morphine (10 mg/kg, s.c.) and fentanyl (50 micrograms/kg, s.c.) in mice. In the tail pinch test, nor-BNI partially antagonized morphine and fentanyl analgesia, but not U-50488H analgesia in the first 30 min after s.c. administration. However, the kappa-antagonistic action gradually increased, reaching a plateau at 2 hr. This antagonistic action was maintained for at least 4 days. In contrast, the mu-antagonistic action declined to the control level at 2 or 4 hr after nor-BNI administration. In the acetic acid-induced writhing test, nor-BNI also exerted a more potent and selective kappa-antagonistic action at 24 hr than at 1 hr after its s.c. administration. Nor-BNI also showed a long-lasting kappa-antagonism against the hyperthermic response induced by U-50488H (5 mg/kg, s.c.). Thus, we found that nor-BNI is a slow-onset, long-lasting, selective kappa-antagonist in vivo.
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PMID:Nor-binaltorphimine: a potent and selective kappa-opioid receptor antagonist with long-lasting activity in vivo. 132 32

Dynorphin A-(1-13)-Tyr-Leu-Phe-Asn-Gly-Pro (Dyn Ia; 1-8 nmol) injected intracerebroventricularly in the mouse produces two independent behavioral effects: (1) a norbinaltorphimine (kappa opioid antagonist)-reversible analgesia in the acetic acid-induced writhing test and (2) motor dysfunction characterized by wild running, pop-corn jumping, hindlimb jerking and barrel rolling and antagonized by the irreversible phencyclidine (PCP) and sigma (sigma) receptor antagonist, metaphit and the non-competitive N-methyl-D-aspartate (NMDA) receptor antagonists, dextromethorphan and ketamine. The specific involvement of the PCP receptor in the motor effects of Dyn Ia is supported by the direct competitive interaction of the peptide with the binding of [3H]MK-801 (Ki: 0.63 microM) and [3H]TCP (Ki: 4.6 microM) to mouse brain membrane preparations.
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PMID:Selective involvement of kappa opioid and phencyclidine receptors in the analgesic and motor effects of dynorphin-A-(1-13)-Tyr-Leu-Phe-Asn-Gly-Pro. 135 18

Antinociceptive actions and effects of intracerebroventricular (i.c.v.) dynorphin-(1-13) (DYN) on morphine (MOR) analgesia and acute tolerance were studied in male Sprague-Dawley rats. Antinociceptive effect against hind paw pressure was produced by 30 micrograms of DYN, but not by 0.5-10 micrograms. Acetic acid writhing was inhibited dose-dependently by DYN at the doses of 2-30 micrograms, and the order of potency of the anti-writhing effect was beta-endorphin > MOR > DYN >> Met-enkephalin. The anti-writhing effect of DYN that was partially antagonized by naloxone at 10 mg/kg, s.c. in MOR tolerant rats was the same as that in MOR naive rats. The anti-writhing effect of i.c.v.-MOR was increased synergistically by DYN. Continuous s.c. (6 mg/kg/hr) and i.c.v. (7.5 micrograms/rat/hr) infusion of MOR produced antinociception against hind paw pressure, which reached maximum (MAX) and attenuated thereafter during MOR infusion for 6 hr. The attenuation of antinociception was also produced during MOR infusion combined with multiple i.c.v.-injection of DYN. The MAX and area under the antinociceptive curve during MOR infusion was not affected by multiple injection of DYN, i.e., no effect of i.c.v.-DYN on the development of acute MOR tolerance induced by s.c.- and i.c.v.-infusion was observed. In conclusion, the anti-writhing effect of i.c.v.-DYN might not be mediated via mu-receptors, although DYN increased the anti-writhing effect of i.c.v.-MOR synergistically and the development of acute tolerance to MOR (i.c.v., s.c.) was not affected by i.c.v.-DYN.
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PMID:Dynorphin-(1-13): antinociceptive action and its effects on morphine analgesia and acute tolerance. 136 87


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