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  • 1
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of medicinal chemistry 13 (1970), S. 143-144 
    ISSN: 1520-4804
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 2 (1975), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Prostaglandin E1 (0·4 mg/kg, i.p.) significantly potentiated the antinociceptive action of morphine in albino rats.2. This potentiation was significantly inhibited by pretreatment with reserpine, p-chlorophenylalanine or methysergide but not by α-methyl-p-yrosine, phentolamine or propranolol.3. The results suggest that the potentiation of morphine by prostaglandin E1 is mediated by serotonin, since it is inhibited by pharmacological agents known to reduce central turnover of serotonin receptors.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 5 (1978), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Five prostaglandin synthesis inhibitors, indomethacin, diclofenac, mefenamic acid, ibufen and paracetamol, were found to inhibit the antinociceptive action of morphine without affecting the antinociceptive response of an equi-analgesic dose of prostaglandin E12. Diclofenac was found to be the most potent and longest acting, whereas paracetamol was the least potent and shortest acting. Indomethacin, mefenamic acid and ibufen occupied an intermediate position, both in potency and duration of action.3. The results suggest that prostaglandins may be involved in the antinociceptive action of morphine in albino rats.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 4 (1977), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The antinociceptive effect of prostaglandins E1, E2 and F2α 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 F2α (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.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Naturwissenschaften 59 (1972), S. 651-651 
    ISSN: 1432-1904
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Naturwissenschaften 59 (1972), S. 650-651 
    ISSN: 1432-1904
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 56 (1978), S. 235-237 
    ISSN: 1432-2072
    Keywords: Pentylenetetrazol ; Clonic convulsions ; PGE1 ; PGF2α ; Serotonin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Prostaglandin E1-(PGE1-) induced inhibition of pentylenetetrazol (PTZ) convulsions in rats were significantly antagonized after pretreatment with drugs known to reduce brain serotonin activity, but not by pharmacological agents that decrease brain catecholamine activity. PGF2α also significantly inhibited PGE1 action. The results suggest that PGE1-induced inhibition of PTZ convulsions is not a direct effect, but an indirect one mediated through increase in brain serotonin activity.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-2072
    Keywords: Antinociception ; PGE1 ; 5,6-Dihydroxytryptamine ; Serotonin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It is generally accepted that prostaglandins (PGs) are nociceptive substances. However, earlier studies from this laboratory indicated that morphine analgesia, in the rat, was not only serotonin mediated, but involved PGs as well. Several PG synthesis inhibitors were shown to inhibit morphine analgesia and PGE1 was shown to potentiate the antinociceptive effect of morphine. Intraperitoneal administration of PGE1, but not PGE2 and PGF2α, elicited antinociceptive effect per se, by the radiant heat method. The present study was undertaken to confirm the antinociceptive action of PGE1, after intracerebroventricular administration, against nociceptive impulses induced by radiant heat, pressure, and high frequency electric current. PGE1 produced a dose-dependent antinociceptive effect by the radiant heat and pressure methods. It potentiated the antinociceptive action of morphine by the electrical stimulation method. The antinociceptive action of PGE1 was not evident in 5,6-dihydroxytryptamine-pretreated rats, suggesting that this effect is serotonin mediated. The present study thus confirms the antinociceptive action of PGE1 and suggests that, unlike its peripheral action, the central action of PGE1 results in suppression of nociceptive responses which may be serotonin mediated.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 73 (1981), S. 157-160 
    ISSN: 1432-2072
    Keywords: Immobilization stress ; Ambient temperature ; Hypothermia ; Hyperthermia ; Brain monoamines
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Immobilization of albino rats for 2 h showed ambient temperature-dependent changes in rectal temperature, hypothermia at temperatures below 30° C, and hyperthermia at 35° C and above. Adrenalectomized (Adre) rats showed more hypothermia compared to sham operated controls at 25±2° C. The increased hypothermia in adrenalectomized rats was reversed by 10 mg/kg IP or 100 μg/rat ICV of hydrocortisone. Groups of rats pretreated with desmethylimipramine (DMI, 25 mg/kg IP) and 6-hydroxydopamine (6-HD, 100 μg/rat ICV) or methyl ester of parachlorophenylalanine (ME-PCPA, 100 μg/rat ICV for 3 days) or 5,6-dihydroxytryptamine (DHT, 75 μg/rat ICV) showed significantly less hypothermia at the end of 2 h of immobilization. Applying analysis of variance test, the hypothermia in Adre, ME-PCPA and DHT groups, was found to be not significantly different from their respective control groups between 0 to 45 min of immobilization but was significantly different between 45 to 120 min of immobilization. DMI-6-HD group however, showed significant difference between 0–45 min only and not between 45–120 min of immobilization. The results suggest that the early phase of immobilization induced hypothermia between 0–45 min is dopamine and the late phase of hypothermia between 45–120 min is 5-hydroxytryptamine mediated.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary PGE1 potentiated, while diclofenac, a prostaglandin synthesis inhibitor, antagonized hexobarbitone hypnosis in rats. PGE1-induced potentiation of hexobarbitone sleep was inhibited by a 5HT synthesis inhibitor and by a 5HT receptor blocker, suggesting that this potentiation is 5HT mediated.
    Type of Medium: Electronic Resource
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