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  • Title: [Interactions between buprenorphine, narcotic analgesic, and centrally acting drugs in prolongation of halothane-induced sleeping and analgesia (author's transl)].
    Author: Yasuda Y, Shioya Y, Nakai S, Shintani S, Hiyama T.
    Journal: Nihon Yakurigaku Zasshi; 1982 Mar; 79(3):163-72. PubMed ID: 6123474.
    Abstract:
    Interactions between buprenorphine, narcotic analgesic, and centrally acting drugs were studied in prolongation of halothane-induced sleeping and analgesia using the D'Amour-Smith method in mice, and the effect of buprenorphine on monoamine metabolism was studied in rat brain. Diazepam and chlorpromazine prolonged the halothane-induced sleeping time dose-dependently. Buprenorphine (0.01, 0.1, and 1 mg/kg s.c.) inhibited the effect of diazepam, but not that of chlorpromazine. Pentazocine and naloxone also inhibited the effect of diazepam, but morphine did not. It is suggested that the inhibitory effect of buprenorphine on prolongation of halothane-induced sleeping time by diazepam is due to its opiate antagonistic property. Since narcotic antagonists inhibited the effect of diazepam, the endogenous opiate system seems to be involved in this effect. Diazepam or droperidol had no effect on the analgesia of buprenorphine, morphine, and pentazocine. Buprenorphine analgesia was inhibited by reserpine and p-chlorophenylalanine, potentiated by 5-hydroxytryptophan, and not affected by alpha-methyl-p-tyrosine or 3,4-dihydroxyphenylalanine. These results suggest that the serotonergic system plays a modulating role in buprenorphine analgesia. Imipramine and nialamide inhibited buprenorphine analgesia in the test at low stimulus intensity, but potentiated at high stimulus intensity. Buprenorphine (0.1, 1 and 10 mg/kg s.c.) increased the dopamine metabolites, 3,4-dihydroxyphenylacetic acid and homovanillic acid, in various brain areas and the serotonin metabolite, 5-hydroxyindoleacetic acid, in midbrain.
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