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Reevaluation of the Effect of Phenobarbital on the Response to Pain in Rat
소병겸,김기원,고명규,양원모,조규박,So, Byoung-Gyoum,Kim, Kee-Won,Ko, Myoung-Kyu,Yang, Won-Mo,Cho, Kyu-Park The Korean Society of Pharmacology 1986 대한약리학잡지 Vol.22 No.2
백서에서 열판법을 이용하여 과민동통을 일으키는 약물로 알려진 phenobarbital의 동통에 대한 효과를 재검토하고 그 기전을 알고저 phenobarbital 단기 또는 장기처리에 의한 뇌내 ${\beta}-endorphin$함량, opiate 수용체 및 시험관내 실험으로 functional opiate 수용체의 변동유무를 검토하여 다음과 같은 결과를 얻었다. 1) 마취에 미달하는 용량의 phenobarbital 1회 복강내 투여는 일시적인 HPL단축에 이어 이를 지연시켰고 phenobarbital 장기 처리는 HPL을 현저히 지연시켰다. 2) Naloxone 자체는 HPL을 현저히 단축시켰고, naloxone처리는 phenobarbital의 HPL 지연 효과를 억제하였다. 3) Phenobarbital 1회 복강내 투여는 뇌내 ${\beta}-endorphin$ 함량에 영향을 미치지 못하였으나 phenobarbital 장기처리는 이를 현저히 증가시켰다. 4) Phenobarbital 1회 복강내 투여는 [3H]-morphine binding에 영향을 미치지 못하였으나, phenobarbital 장기처리는 Kd치와는 달리 Bmax를 현저히 감소시켰다. 5) Phenobarbital 장기처리에 의한 HPL변동, 뇌내 ${\beta}-endorphin$함량변동 그리고 opiate receptor Bmax변동 삼자간에는 유의한 상관관계가 있었다. 6) 적출vas deferens 표본에서 phenobarbital 장기처리는 morphine의 ID50은 증가시키고 maximum effect는 감소시키나 naloxone에 대한 $pA_2 $치에는 영향을 미치지 못하였다. 이상의 실험성적은 phenobarbital이 일시적인 과민동통 효과에 이어 진통효과를 갖고 있으며, phenobarbital의 진통효과는 뇌내 ${\beta}-endorphin$함량 증가와 이로 인한 functional opiate 수용체의 숫적 변동에 기인함을 시사하였다. Clinically, subhypnotic doses of barbiturates have been known to elicit hyperalgesia. In this experiment, effect of acute or chronic phenobarital treatment on the response to pain in rat was reevaluated by hot-plate method. To elucidate its mechanism, changes of ${\beta}-endorphin$ contents and [3H]-morphine binding of the rat midbrain as well as functional opiate receptor in vas deferens were also measured. Intraperitoneal injection of sub anesthetic dose phenobarbital induced initial hyperalgesia followed by successive analgesia, while chronic phenobarbital-treatment decreased reactivity to pain. Naloxone (10mg/kg, i.p.) markedly shortened hot plate latency period, and significantly inhibited the analgesic action of phenobarbital. Single dose of phenobarbital did not affect ${\beta}-endorphin$ contents and [3H]-morphine binding in rat mid brain, but in the chronic phenobarbital-treated groups, ${\beta}-endorphin$ contents was increased, while Bmax of opiate receptor binding was decreased. Moreover, very significant correlations among responses to pain, changes of ${\beta}-endorphin$ contents and opiate receptor binding were observed. However, Kd values of opiate receptor bindings were not changed in all preparations. In the chronic phenobarbital-treated vas deferens preparations, ID50 of morphine was increased witb concomittant decrease of maximum effect. But $pA_2 $, value for naloxone was not changed. From these results, it is suggested that phenobarbital can produce analgesia due to changes of ${\beta}-endorphin$ contents as well as functional opiate receptors by receptor regulation.
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白鼠에서 疼痛에 미치는 Phenobarbital 效果의 再評價
소병겸,이화옥,김기원,조규박,은홍배 전북대학교 의과학연구소 1986 全北醫大論文集 Vol.10 No.4
Clinically, subhypnotic doses of barbiturates have been known to elicit hyperlgesia. In this experiment, effect of acute or chronic phenobarbital on the response to pain in rats was reevaluated by hot-plate method. To elucidate its mechanism, changes in β-endorphin contents and [^3H]-morphine binding of the rat midbrain as well as functional opiate receptor in vas deferens were also measured. Intraperitoneal injection of subanesthetic dose of phenobarbital induced initial hyperalgesia followed by successive analgesia, while chronic phenobarbital-treatment decreased reactivity to pain. Naloxone(10mg/kg, I. p.) markedly shortened hot plate latency, and significantly inhibited the analgesic action of phenobarbital. Single dose of phenobarbital did not affect β-endorphin contents and [^3H]-morphine binding in rat madbrain, but in the chronic phenobarbital-treated groups, β-endorphin content was increased, while Bmax of opiate receptor binding was decreased. Moreover, very significant correlations among response to pain, changes in β-endorphin contents and opiate receptor binding were observed. However, Kd values of opiate receptor binding swere not changed in all preparations. In the chronic phenobarbital-treated vas deferens preparation, ID_50 of morphine was increased with concomitant decrease of maximum effect. But pA_2 value for naloxone was not changed. From these resuts, it is suggested that phenobarbital can produce analgesia due to changes in β-endorphin contents as well as functional opiate receptors by receptor regulation.
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백서에서 동통에 미치는 Phenobarbital 효과의 재평가
소병겸(Byoung-Gyoum So),김기원(Kee-Won Kim),고명규(Myoung-Kyu Ko),양원모(Won-Mo Yang),조규박(Kyu-Park Cho) 대한약리학회 1986 대한약리학잡지 Vol.22 No.2
Clinically, subhypnotic doses of barbiturates have been known to elicit hyperalgesia. In this experiment, effect of acute or chronic phenobarital treatment on the response to pain in rat was reevaluated by hot-plate method. To elucidate its mechanism, changes of β-endorphin contents and [3H]-morphine binding of the rat midbrain as well as functional opiate receptor in vas deferens were also measured. Intraperitoneal injection of sub anesthetic dose phenobarbital induced initial hyperalgesia followed by successive analgesia, while chronic phenobarbital-treatment decreased reactivity to pain. Naloxone (10mg/kg, i.p.) markedly shortened hot plate latency period, and significantly inhibited the analgesic action of phenobarbital. Single dose of phenobarbital did not affect β-endorphin contents and [3H]-morphine binding in rat mid brain, but in the chronic phenobarbital-treated groups, β-endorphin contents was increased, while Bmax of opiate receptor binding was decreased. Moreover, very significant correlations among responses to pain, changes of β-endorphin contents and opiate receptor binding were observed. However, Kd values of opiate receptor bindings were not changed in all preparations. In the chronic phenobarbital-treated vas deferens preparations, ID50 of morphine was increased witb concomittant decrease of maximum effect. But pA<sub>2</sub> , value for naloxone was not changed. From these results, it is suggested that phenobarbital can produce analgesia due to changes of β-endorphin contents as well as functional opiate receptors by receptor regulation. 백서에서 열판법을 이용하여 과민동통을 일으키는 약물로 알려진 phenobarbital의 동통에 대한 효과를 재검토하고 그 기전을 알고저 phenobarbital 단기 또는 장기처리에 의한 뇌내 β-endorphin함량, opiate 수용체 및 시험관내 실험으로 functional opiate 수용체의 변동유무를 검토하여 다음과 같은 결과를 얻었다. 1) 마취에 미달하는 용량의 phenobarbital 1회 복강내 투여는 일시적인 HPL단축에 이어 이를 지연시켰고 phenobarbital 장기 처리는 HPL을 현저히 지연시켰다. 2) Naloxone 자체는 HPL을 현저히 단축시켰고, naloxone처리는 phenobarbital의 HPL 지연 효과를 억제하였다. 3) Phenobarbital 1회 복강내 투여는 뇌내 β-endorphin 함량에 영향을 미치지 못하였으나 phenobarbital 장기처리는 이를 현저히 증가시켰다. 4) Phenobarbital 1회 복강내 투여는 [3H]-morphine binding에 영향을 미치지 못하였으나, phenobarbital 장기처리는 Kd치와는 달리 Bmax를 현저히 감소시켰다. 5) Phenobarbital 장기처리에 의한 HPL변동, 뇌내 β-endorphin함량변동 그리고 opiate receptor Bmax변동 삼자간에는 유의한 상관관계가 있었다. 6) 적출vas deferens 표본에서 phenobarbital 장기처리는 morphine의 ID50은 증가시키고 maximum effect는 감소시키나 naloxone에 대한 pA<sub>2</sub> 치에는 영향을 미치지 못하였다. 이상의 실험성적은 phenobarbital이 일시적인 과민동통 효과에 이어 진통효과를 갖고 있으며, phenobarbital의 진통효과는 뇌내 β-endorphin함량 증가와 이로 인한 functional opiate 수용체의 숫적 변동에 기인함을 시사하였다.
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