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가토에서 혈압에 관여하는 약물의 작용에 대한 니페디핀의 영향
고석태(Suk Tai Ko),정창주(Chang Ju Jung),김해석(Hai Suk Kim) 대한약학회 1992 약학회지 Vol.36 No.4
In order to investigate the effect of nifedipine, Ca2+ channel antagoninst, on the action of some drugs participating in blood pressure, this experiment was performed in rabbits. Nifedipine decreased the pressor actions of norepinephrine, angiotensin and carotid artery clamping, but did not affect the pressor actions of tyramine and depressor actions of acetylcholine and pilocarpine. Nifedipine inhibited the potentiated pressor action of norepinephrine and angiotensin, but did not influence the potentiated pressor action of tyramine in rabbits pretreated with chlorisondamine, ganglionic blocking agent. Nifedipine weakened the potentiated pressor action of norepinephrine, did not affect the pressor action of angiotensin and the potentiated pressor action of tyramine in rabbits pretreated with debrisoquine, sympathetic neuronal blocking agent.
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Debrisoquine이 노르에피네프린 및 티라민의 승압효과에 미치는 영향
고석태(Suk Tai Ko),김해석(Hai Suk Kim),이상현(Sang Hyan Lee) 대한약학회 1986 약학회지 Vol.30 No.3
The influence of debrisoquine on pressor actions of norepinephrine (NE) and tyramine (TR) was investigated in rabbits. Debrisquine(D), in the doses of 1.0, 3.0 and 6.0mg/kg, I.v. potentiated significantly the pressor actions of NE and TR, except the action of TR in the dose of 1.0 mg/kg of debrisoquine. NE response potentiated by debrisoquine was not affected by tranylcypromine, a MAO inhibiter, or desipramine, a NE uptake blocking agent, but augmented by reserpine, a NE depleting agent, or bethanidine, a sympathetic neuronal blocking agent. NE response potentiated by tranylcypromine or desipramine was augmented by debrisoquine, while NE response potentiated by reserine or bethanidine was not affected by debrisoquine. TR response potentiated by debrisoquine was weakened by tranylcypromine, desipramine or reserpine, and not affected by bethanidine. TR response in rabbit pretreated with tranylcypromine, desipramine or reserpine was augmented by debrisoquine, but in rabbit pretreated with bethanidine was not affected by debrisoquine.
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alpha2-아드레날린 효능약인 UK 14,304의 신장기능에 미치는 영향
고석태(Suk Tai Ko),김해석(Hai Suk Kim),최홍석(Hong Seok Choi) 대한약학회 1997 약학회지 Vol.41 No.4
The effects of UK 14,304, an alpha2-adrenergic agonist, on renal function were investigated in dogs. UK 14,304, when given intravenousely(15.0mcg/kg, 50mcg/kg), produced the increase of urine flow accompanied with the marked augmentation of free water clearance (CH2O) and reabsorption rates of sodium in renal tubules (RNa), and the remarkable decrease of osmolar clearance (Cosm) and the amounts of sodium excreted in urine (ENa). UK 14,304 given into a renal artery(l.5mcg/kg, 5.0mcg/kg) elicited the increase of urine flow with the augmentation of CH2O in both kidney. UK 14,304, when administered into carotid artery(3.0mcg/kg, 10.0mcg/kg). exhibited the same aspect as shown in intravenous UK 14.304 at smaller dose than the intravenous dose. Diuretic action of intravenous UK 14,304 were produced together with increase of CH2O in situation of water diuresis too, changes of renal function in this state were the increase of Cosm, ENa, and EK (excreted amounts of potassium in urine), and the decrease of RNa and RK, these were different appearances from situation of saline diuresis. Diuretic action of intravenous UK 14,304 were blocked completely by post or pretreatment of yohim-bine, alpha2-adrenergic blocking agents, and inhibited by pretreatment of vasopressin, antidiuretic hormone. Above results suggest that UK 14,304 produces the diuretic action by the inhibition of vasopressin secretion and suppression of electrolytes reabsorption of electrolytes in renal tubules mediated with central alpha2-adrenoceptor in dog.
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α₂-아드레날린 효능약인 UK 14,304의 신장기능에 미치는 영향
고석태,김해석,최홍석 朝鮮大學校 1998 藥學硏究誌 Vol.19 No.2
The effects of UK 14,304, an α₂-adrenergic agonist, on renal function were investigated in dogs. UK 14,304, when given intravenousely(15.0 μg/kg, 50μg/kg), produced the increase of urine flow accompanied with the marked augmentation of free water clearance(C_(H₂O)) and reabsorption rates of sodium in renal tubules (R_(Na)), and the remarkable decrease of osmolar clearnance (C_(osm)) and amounts of sodium excreted in urine (E_(Na)). UK 14,304 given into a renal artery(1.5 μg/kg, 5.0μg/kg) elicited the increase of urine flow with the augmentation of C_(H₂O) in both kidney. UK 14,304. when administered into carotid artery(3.0μg/kg. 10.0μg/kg). exhibited the same aspect as shown in intravenous UK 14,304 at smaller dose than the intravenous dose. Diuretic action of intravenous UK 14,304 were produced together with increase of C_(H₂O) in situation of water diuresis too. changes of renal function in this state were the increase of C_(osm), E_(Na), and E_(K) (excreted amounts of potassium in urine), and the decrease of R_(Na) and R_(K), these were different appearances from situation of saline diuresis. Diuretic action of intravenous UK 14,304 were blocked completely by post or pretreatment of yohim-bine. α-adrenergic block agent. And inhibited by pretreatment of vasopressin. antidiuretic hormone. Above results suggest that UK 14,304 produces the diuretic action by the inhibition of vasopressin secretion and suppression of electrolytes reabsorption of electrolytes in renal tubules mediated with central α₂-adrenoceptor in dog.
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고석태,김해석,유강준 한국응용약물학회 1993 Biomolecules & Therapeutics(구 응용약물학회지) Vol.1 No.1
This study was performed to elucidate the mechanism of antidiuretic action of diltiazem by infusion into the vein and carotid artery, of diuretic action into a renal artery in dog. Renal denervation caused a reversal of the effect of diltiazem from the antidiuretic to the diuretic when infused into vein or carotid artery, and potentiated the diuretic effect when infused into a renal artery. The changes of renal function in diuretic circumstances as described above included the increase in renal plasma flow, osmolar clearance, the amounts of sodium and potassium excreted in urine and the decrease in reabosrption rate of sodium and potassium in renal tubules. Above results suggest that antidiuretic action of diltiazem may be mediated by central nervous system, not by endogenous substance, diuretic action by direct renal action.
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高錫太,金海石,柳康俊 조선대학교 약학연구소 1993 藥學硏究誌 Vol.15 No.1
Enalapril, angiotensin converting enzyne(ACE) inhibitor, when injected into the vein in dog, produced diuretic action accompanied with the icrease of renal plasma flow(RPF), glomerular filtration rate (GFR), osmolar substance clearace(Cosm) and excretion rates of sodium and potassium in urihne(E_Na, E_K), but in this time, reabsorption rates of sodium and potassium in renal tubules(R_Na, R_K) were not changed at all. Enalapril, when infused into carotid artery, exhibited the same aspect with changes of renal function by intravenous enalapril. Enalapril infused into a renal artery did not affect the renal function of experimental kidney as a matter of control kidney. Above resalts suggest that enalapril produced diuretic action by renal hemodynamic inprovement through the central function
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