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김연진,조백현,송윤강,곽용근,조규박 의과학연구소 1988 全北醫大論文集 Vol.12 No.2
In this study, the effect of ketamine on the response to painful stimuli and modification by some antagonists to norepinephrine serotonin and opiate receptors were investigated in rats. And also, the influence of ketamine on the [^3H]-naloxone binding in vitro and on the plasma β-endorphin content were determined. Ketamine(30-120mg/kg, i.p.) increased the tail-flick latency(TFL), measured by tail immersion method, in dose-dependent manner. This analgesic action of ketamine was significantly inhibited by pretreatment of phentolamine(10mg/kg, i.p., ID50=0.49±0.03mg/kg), naloxone and methysergide(0.1-10mg/kg, i.p., ID50=0.064±0.005mg/kg), respectively. The analgesic action of ketamine was greatly potentiated in the reserpine-pretreated rats(1mg/kg, i.p., for 6 days), while the effect of ketamine was almost abolished in the p-chloro-phenylalanine-pretreated animals(300mg/kg, i.p., once 2 days before experiment). In a radioligand binding assay with (^3H)-naloxone, ketamine(0.3-300uM) produced dose related inhibition of [^3H]-naloxone binding in vitro. The inhibitory potency of ketamine on [^3H]-naloxone binding was far weaker than that of morphine or naloxone. Intraperitoneal ketamine(60mg/kg)-induced increase of the plasma immunoreactive β-endorphin content was significantly inhibited by methysergide(1mg/kg, i.p.,) pretreatment, while that not influenced by phentolamine (10mg/kg). These results suggest that the analgesic effect of ketamine is due to at least three possible mechanisms ; central sympathetic nervous system which modify pain perception, direct agonistic action to opiate receptor and increase of β-endorphin content by central serotoninergic system.
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剔出 白鼠 Vas Deferens에서 5-Hydroxytryptamine의 筋收縮 機轉에 關한 硏究
안효숙,우영종,송윤강,김용기,김기원,조규박 의과학연구소 1987 全北醫大論文集 Vol.11 No.4
To elucidate the mechanisms of contractile action of 5-hydroxytryptamine(5-HT) on the smooth muscle, the effects of 5-HT, norepinephrine(NE) or tyramine on rat vas deferens smooth muscle were studied in vitro comparatively, and also analyzed the effects of 5-HT on efflux of (^3H)-norepinephrine from this preparation. Results obtained from this experiments were summerized as fellows : 1 . 5-HT. NE and tyramine caused contractile response of isolated vas deferens in dose dependent manner. Fashion of muscle contraction induced by 5-HT was resembled to that of tyramine. In addition, phentolamine reduced the effects of 5-HT and tyramine at concentration lower than those necessary to antagonize NE-induced effects. 2 . After pretreatment with cyproheptadine, the effects of 5-HT(in lower doses of 5-HT)were significantly inhibited. But the effects of NE or tyramine were not affect. 3. Cocaine potentiated the effects of NE ana lower doses of 5-HT, but signiiicantly reduced the effects of tyramine and high doses of 5-HT. 4. In vas deferens preparations from reserpinized rats, the effects of NE and lower doses of 5-HT were potentiated, on the contrary the contractile effects of high doses of 5-HT were diminished, and the effect of tyramine was almost completely abolished. 5. In receptor protection experiments, when protection was performed by NE, response to NE was protected from phenoxybenzamine more effectively than that of 5-HT. While when 5-HT was used as protecting agent, response to 5-HT was protected more effectively than that of NE. 6. The effects of 5-HT on the efflux of [^3H]-norepinephrine from rat vas deferens were different according to doses of 5-HT. The efflux of radioactivity was increased by relatively high dose of S-HT but not effected by low doses of 5-HT. These results suggest that there are at least three mechanisms responsible to contractile action of 5-HT in the isolated vas defens preparation ; direct action on 5-HT receptor(possibly"D"), direct activation of α-adrenoceptor and another one is through being taken up into sympathetic nerve terminals and causing the release of NE from the storage sites.
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