• The Journal of Internal Korean Medicine
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• v.21 no.3
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• pp.467-475
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• 2000

The water extracts of Jagamcho-tang has been used for treatment of arrhythmia and palpitation in oriental traditional medicine. Brain is provided with blood flow by heart. Jagamcho-tang has been studied on ischemia and infarction in heart. However, little is known about the mechanism by which the water extracts of Jagamcho-tang rescues brain cells from ischemic damages. To elucidate the protective mechanism on ischemic induced cytotoxicity, the effects of Jagamcho-tang on ischemia induced cytotoxicity and generation of nitric oxide(NO) are investigated in C6 glioma cells. Jagamcho-tang induce NO in a dose dependent manner up to 2.5mg/ml in C6 glioma cells. The pretreatment of Jagamcho-tang protect sodium nitroprusside(SNP) (2mM) induced cytotoxicity. This effect of Jagamcho-tang is mimicked by treatment by pretreatment of SNP($100{\mu}M$), an exogenous NO donor. NG-monomethyl-L-arginine($N^{G}MMA$), a specific inhibitor of nitric oxide synthase (NOS), significantly blocks the protective effects of Jagamcho-tang on cell toxicity by ischemia. In addition, lipopolysaccharide(LPS) and phorhol 12 myristate 13-acetate(PMA) treatment for 72h in C6 glial cells markedly induce NO, but treatment of the cells with the water extracts of Jagamcho-tang decrease nitrite formation in a dose dependent manner. In addition, LPS and PMA treatment for 72h induce severe cell death and LDH release into medium in C6 glial cells. However treatment of the cells with the water extracts of Jagamcho-tang dose not induce significant changes compare to control cells. Furthermore, the protective effects of the water extracts of Jagamcho-tang is mimicked by treatment of $N^{G}MMA$. Taken together, I suggest that the protective effects of the water extracts of Jagamcho-tang against ischemic brain damages may be mediated by regulation of iNOS during ischemic condition.

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.5
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• pp.1449-1455
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• 2004

Bufonis venenum (dried toad venom; Chinese name, Chan su) is a traditional Chinese medicine obtained from the skin venom gland of the toad. It has long been used in treating arrhythmia and other heart diseases in China and other Asian countries. Additionally, Bufonis venenum has been reported to selectively inhibit the growth of various lines of human cancer cells. In the present study, it was examined the effects of extract of Bufonis venenum (EBV) on the growth of human bladder carcinoma cell line T24 in order to investigate the anti-proliferative mechanism and induction of apoptosis by EBV. Treatment of T24 cells to EBV resulted in the growth inhibition, morphological change and induction of apoptotic cell death in a dose-dependent manner. Flow cytometric analysis revealed that EBV treatment caused G2/M phase arrest of the cell cycle and down-regulation of cyclin A, cyclin B1 and Cdc2, which was associated with a marked up-regulation of cyclin-dependent kinases (Cdks) inhibitor p21 (WAF1/CIP1) in a p53-independent manner. The Cdc25C expression was also significantly inhibited by EBV treatment, however Wee1 kinase expression was not affected. The induction of apoptotic cell death by EBV was connected with down-regulation of anti-apoptotic Bcl-XS/L expression without alteration pro-apoptotic Bax expression. Taken together, these findings suggest that EBV may be a potential chemotherapeutic agent for the control of human bladder carcinorma cells and further studies will be needed to identify the active compounds that confer the anti-cancer activity of EBV.

• Journal of Chest Surgery
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• v.38 no.11 s.256
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• pp.776-779
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• 2005

Anomalous origin of right coronary artery from left sinus of valsalva is associated with sudden unexpected death, syncope, arrhythmia and myocardial ischemia. The mechanism that explains the restriction of coronary flow in the anomalous coronary artery is unclear but several surgical methods have been proposed, such as coronary artery bypass graft, coronary reimplantation, translocation of pulmonary artery, and unroofing procedure. We reported the surgical correction of the anomalous origin of right coronary artery from left sinus of valsalva between the aorta and pulmonary trunk using the unroofing procedure.

• Journal of Chest Surgery
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• v.34 no.11
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• pp.809-822
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• 2001

Background: Ischemic preconditioning(IP) is known to be effective in the protection of myocardial necrosis, arrhythmia, and the restoration of the myocardial function in the ischemia-reperfusion state of the heart. However the exact mechanism is not clearly understood. The purpose of this study was to elucidate the trigger mechanism 7f IP on the restoration of the myocardial function after ischemia-reperfusion. Material and Method: By connecting a Langendorff perfusion apparatus with an isolated heart of a rat, the normal temperature of the heart was maintained. The experiment was conducted in seven groups, which were divided according to the preconditioning stimuli and blockage methods Group I(n=10) was a group without IP, Group II(n=10) a group of three-minute IP, Group III(n=10) a group of PEIP, Group IV(n=10) a group of clonidine IP, Group V(n=10) a group of If after reserpine, Group Vl(n=10) a group of PE & prazosin IP, and Group Vll(n=10) a group of clonidine & yohimbine IP. Hemodynamic parameters of DP, LVEDP, $\pm$dP/dT and the changes of perfusion in the coronary artery were evaluated. Result: Developed pressure and +dP/dT changed per unit time. After 20 minutes of reperfusion, those of Group II and III were 63.1$\pm$3.7%, 64.8$\pm$4.6% and 64.5$\pm$4.6%, 63.8$\pm$4.4%, which improved more significantly than those of Group I(P<0.05), However, there were no significant differences between the Groups V and Vl, and Group I. Conclusion: The Brief ischemic preconditioning and pharmacological preconditioning using $\alpha$-receptor sympatho-mimetics have protecting effects on the restoration of myocardial function after reperfusion. And the protecting effect of preconditioning seems to be related to sympathetic neurotransmitters and to the selective action of the $\alpha$$_1$-adrenergic receptor.

• Journal of Yeungnam Medical Science
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• v.8 no.2
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• pp.52-62
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• 1991

The toxic effect of azalea extract, expecially on cardiovascular system, is relatively unclear. The purpose of this study is to study the possible underlying mechanism and effect of toxic ingredient of azalea on cardiovascular system. The 71 healthy rabbits were divided into 10 groups : In group as preliminary study ; 4cc of normal saline was administered intravenously(N) ; 0.7gm/kg and 1.0gm/kg of azalea extract was administered respectively in the same route, volume(A1, A2) ; atropine was administered intravenously(A) ; after pretreatment with atropine(0.04mg/kg) to block parasympathetic system, azalea extract was injected like the above groups(AA1, AA2) ; normal saline, 0.7gm/kg and 1.0gm/kg of azalea extract were administered respectively with 0.2cc(1 : 1000) epinephrine(E0,E1,E2). We measured the following indices at I minute interval during first 10 minutes and then 10 minute interval during next 30 minutes : RR interval, QTc interval, maximal systolic and diastolic pressure drop with occuring time and presence of significant arrhythmia. The results were as follows : 1. The changes of RR interval, QTc interval were significantly increased in groups by Azalea extract. The blood pressure change was significantly decreased in groups by Azalea extract. There were no significant differences according to dosage of Azalea extract. 2. The changes of RR interval, blood pressure were significant differences between administration of atropine and Azalea extract after pretreatment with atropine, but not in the change of QTc interval. 3. There were no significant differences in the change of RR interval, ATc interval, blood pressure drop according to pretreatment with atropine. 4. The interaction between epineprine and Azalea extract was not noted by the effect of epineprine itself. 5. The ST change by 0.7gm/kg, 1.0gm/kg of Azalea extract was revealed in 1 case(14.0%), 7 case(100%), respectively. 6. Most of all cases with arrhthymia, ventricular tachycardia, ventricular fibrillation, were noted in the group by epineprine, except one case by Azalea extract(1.0gm/kg). It was idioventricular rhythm. In conclusion, azalea extract has negative inotropic and chronotropic effect with arrhythmogenic potential possibly through direct myocardial ischemia or injury but we cann't be absolutely exclusive of actions of autonmic nervous system, especially parasympathetic nervous system.