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곽용근,오남휴,김용기,채수완,조규박 의과학연구소 1990 全北醫大論文集 Vol.14 No.2
This study was purposed to evaluate the cardiovascular effect of RU24213 and the interaction between DA_1 and DA_2 activity in anesthetzed cat. The results obtained were as follows; 1. Intravenous or intraventricular RU24213 elicited dose-related hypotension and bradycardia. 2. The hypotensive effect of intravenous Ru24313 was blocked not by intravenous SCH23390 but by intravenous sulpiride, and the bradycardiac effect of intravenous RU24313 was blocked by intravenous SCH23390 or intravenous sulpiride. 3. The cardiovascular effect of intravenous RU24313 was blocked by intravenous phenoxybenzamine, propranolol, hexamethonium or atropine, and bilateral vagotomy did not ihhibit the htpotensive effect of intravenous RU2413 but inhibited bradycardiac effect of the drug. 4. The hypotensive and bradycardisc effects of intravenous RU24213 were inhibited by pretreatment with SKF38393. From the above results. it is suggested that hypotensive effect of RU24313 was developed via central and peripheral dopamine receptors, while bradycardiac effect of the drug was related to the peipheral of DA_1 receptor inhibits the action of DA_2 agonist in cardiovascular system of cat. (Key Wards: RU24213, dopamine D_1, dopamine D_2 receptor, cardiovascular ststem, cat)
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微生物에 依한 石炭酸포화吸着粒狀活性炭의 再生에 관한 硏究
郭龍根,金東潤 부산대학교 환경문제 연구소 1987 環境硏究報 Vol.5 No.-
1. Among three microorganisms including LLMO (trade name, made in U.S.A), KIHARA (trade name, made in Japan), and the activated sludge from the Coca-cola Company in Pusan, the KIHARA resulted in the best efficieny for removal of phenol in aqueous solution. The experiments were carried out in the batch type aerator. 2. Influent with 5ppm of phenol concentration was feeded into the granular activated carbon column which was seeded by the KIHARA. Effluent phenol concentration approached to near zero. 3. It was found that the activated carbon column seeded with KIHARA had resistance to the shock loading, since the effluent phenol concentration was increased in minimal even though the influent phenol concentration was increased to 12 ppm from 5 ppm abruptly.
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백서에서 Morphine의 진통효과에 미치는 Verapamil, Diltazem, Bay K 8644 및 KT 362의 영향
송윤강,곽용근,김기원,조규박,김용기 의과학연구소 1993 全北醫大論文集 Vol.17 No.2
백서에서 피하 또는 뇌실내 verapamil, diltiazem, Bay K 8644 및 KT 362의 진통효과를 검토하고 mor-phine의 진통효과에 미치는 이들 약물들의 영향을 관찰하여 다음과 같은 성적을 얻었다. 1. Morphine은 약물 용량에 비례하여 HPL 증가를 일으켰다. 2. Morphine은 정상 및 고농도의 KCL 자극 midbrain synaptosome에서 약물 용량에 비례하여 ^4^5 Ca^2^+ uptake를 억제하였다. 3. 피하 verapamil(20mg/kg)과 피하 diltiazem(20mg/kg)는 HPL 증가를 일으켰으나 피하 Bay K 8644(1mg/kg)와 피하 KT 362(1mg/kg)는 HPL에 아무런 영향을 미치지 아니하였다. 4. 뇌실내 verapamil(100㎍)과 뇌실내 diltiazem(100㎍)은 현저한 HPL 증가를 일으켰고 뇌실내 KT 362(100Mg)는 HPL에 아무런 영향을 미치지 아니하였다. 5. 피하 verapamil(2mg/kg)과 피하 diltiazem(2mg/kg)은 morphine의 진통작용을 강화하였고 피하 Bay K 8644(1mg/kg)는 morphine의 진통작용을 억제 하였으며 피하 KT 362(5mg/kg)는 morphine의 진통작용에 아무런 영향을 미치지 아니하였다. 이상의 실험성적은 morphine의 진통작용 발현에 Ca^2^+ - channel이 중요한 역할을 하고 있으며, Ca^2^+ - channel 차단제가 단독 또는 morphine과 병합하여 동통치료에 사용될 수 있음을 시사한다. The influences of subcutaneous or intraventricular verapamil, diltiazem, Bay K 8644 or KT 362 on the morphine induced analgesia were investigated by measuring the hot plate latency(HPL) of rats. 1. Morphine elicited dose-dependent analgesia and inhibited ^4^5Ca^2^+ uptake in naive or KCI-stimulated midbrain synaptosomes. 2. Bay K 8644 (1mg/kg, s.c.) or KT 362 (1mg/kg, s.c.) did not affect the HPL, but verapamil (20mg/kg, s.c.) and diltiazem (20mg/kg, s.c.) increased it. 3. Intracerebroventricular verapamil (100㎍) and diltiazem (100㎍) markedly increased the HPL of rat, but intracerebroventricular KT 362 did not affect the HPL. 4. Subcutaneous verapamil (2mg/kg) and diltiazem (2mg/kg) potenitiated the morphine-induced analgesia, while subcutaneous Bay K 8644 (1mg/kg) diminished the analgesic effect of morphine. However, subcutaneous KT 362(5mg/kg) did not affect the analgesic effect of morphine. These results, suggest that calcium channel is playing an important role in mediating the analgesic effect of opiates and that calcium channel blockers might may be clinically applied in controlling pain.
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김기원,곽용근,채준석,조규박,Kim, Kee-Won,Kwak, Yong-Geun,Chae, Joon-Seak,Cho, Kyu-Park The Korean Society of Pharmacology 1987 대한약리학잡지 Vol.23 No.2
Morphine을 비롯한 opioid peptide가 말초 또는 중추에 투여시 혈압하강과 심박동수감소를 보이며 opiate 수용체 길항제인 naloxone에 의해 길항됨이 관찰되었던바 근래 몇몇 보고들은 중추신경내에서 adrenergic및 opioidergic system이 서로 관련되어 있음을 시사하고 있다. 이에 본 실험에서 고혈압 연구에 널리 사용되고 있는 2-kidney, 1-clip (2K1C) 방법으로 실험적 고혈압을 유발시킨 백서의 측뇌실내 clonidine또는 morphine의 심맥관계에 대한 효과와 각각의 차단제에 의한 영향 그리고 정상 및 고혈압상태 백서의 뇌내 ${\beta}-endorphin$의 함량과 specific opiate receptor binding을 정량하여 고혈압 유발에 따른 뇌내 opiate system의 변동을 관찰하였다. 2K1C 고혈압 또는 sham-operated대조백서에서 측뇌실내 clonidine $(3-30\;{\mu}g/kg)$은 용량에 비례하여 혈압하강과 심박동수감소를 일으켰으며 clonidine의 혈압강하 효과는 2K1C고혈압 백서에서 더욱 현저하였다. clonidine의 혈압강하효과는 고혈압 백서에서 측뇌실내 yohimbine 또는 naloxone 전처리에 의해 약화되었고 대조군에서는 yohimbine ($30\;{\mu}g/kg$, i.v.t.)에 의해 억제되었으나 naloxone ($50\;{\mu}g/kg$, i.v.t.)에 의해서는 영향 받지 않았다. clonidine과 마찬가지로 측뇌실내 morphine $(10-100\;{\mu}g/kg)$은 2K1C 고혈압 또는 sham-operated 대조백서에서 용량에 비례하여 혈압하강과 심박동수감소를 일으켰으며, morphine의 혈압강하효과는 2K1C 고혈압백서에서 더욱 현저하였다. 대조군과 고혈압군에서 morphine의 혈압강하효과는 naloxone 전처리에 의해 현저히 약화되었으나 yohimbine에 의해서는 영향 받지 않았다. 2K1C 시술익일부터 투여한 clonidine은 2K1C 시술에 의한 혈압 상승을 억제하였으며 naloxone (2 mg/kg, i.p.)에 의해 반전되었다. 2K1C 시술에 의해 고혈압이 유발된 백서의 뇌내 ${\beta}-endorphin$ 함량은 sham-operated 군에 비하여 유의하게 감소되어 있었고 (3H)-naloxone의 specific binding의 Bmax는 증가되었으나 Kd치는 변동되지 않았다. 이상의 실험 성적은 뇌내 opiate계가 혈압조절에 중요한 역할을 담당하고 있으며 2K1C 고혈압백서의 고혈압상태 유지에 뇌내 opiate계의 기능저하가 일부관여하고 있음을 강력히 시사한다. The possible inolvement of central opiate system in the control of cardiovascular function and in the antihypertensive action of clonidine has been examined in unanesthetized rats with shamoperated or 2-kidney, 1-clip (2K1C) renal hypertension. In both groups of rats, intraventricular clonidine $(3-30\;{\mu}g/kg)$ produced hypotension and bradycardia. Hypotensive action of clonidine was more potent in the hypertensive rats than in the normotensive sham-operated rats. Yohimbine $(30\;{\mu}g/kg,\;i.v.t.)$ inhibited the hypotension and bradycardia produced by clonidine. Naloxone ($50\;{\mu}g/kg$, i.v.t.) inhibited the action of clonidine in 2K1C hypertensive rats but not influenced in the sham-operated rats. Intraventricular morphine $(10-100\;{\mu}g/kg)$ also reduced rats. Intraventricular morphine $(10-100\;{\mu}g/kg)$ also reduced blood pressure and heart rate in both groups of rats. But these effects were not affected by yohimbine, but antagonized by naloxone ($50\;{\mu}g/kg$, i.v.t.). Chronic treatment of 2K1C rats with clonidine ($3{\times}20\;{\mu}g/kg$, p.o.,) for 14 days from 1 day after 2K1C operation) suppressed the development of hypertension and maintained the blood pressure in normal level and this errect of clonidine was abolished by naloxone (2 mg/kg, i. p.). In the 2K1C hypertensive rats, immunoreactive ${\beta}-endorphin$ content was significantly decreased, but maximum binding (Bmax) of $(^3H)-naloxone$ was significantly increased in brain of 2K1C hypertensive rats. However, Kd value was not changed. These results suggest that the opioidergic component might be involved in the antihypertensive action of clonidine only in hypertensive and that central opiate system might play important roles in pathophysiology of development and maintenance of hypertension.
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