• The Korean Journal of Pharmacology
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• v.11 no.1 s.17
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• pp.33-38
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• 1975

The clinical efficacy of Ethaverine, a peripheral vasodilator, was studied according to a double-blind, non-cross over method in 29 diabetic patients with peripheral arterial diseases. The clinical improvement was assessed from the history of patients including the incidence and frequency of intermitten claudication. Ethaverine, after 4 weeks of therapy, was not effective in improving clinical symptoms compared to placebo. Ethaverine, however, was an efective vasodilator than placebo. The quality of vasodilation induced by Ethaverine, was similar to that of alcohol. A new clinical method of studying peripheral vasodilator was presented. The clinical symptoms of peripheral vascular arterial disease in the lower extrimities include reduced intensity of palpable pulses, coldness, and discoloration of the skin. Intermittent claudication may be present. Pathologic changes in vessel architecture precede the symptoms, and recognition of impending vascular insufficiency is a determining factor in selecting vasodilating therapy or surgical management. Also, post-operative patients who have chronic peripheral vascular arterial disease may be candidates for subsequent vasodilating therapy. Peripheral vasodilators, according to the series of reports, may be indicated in vasospastic peripheral vascular condition rather than an occlusive vascular disease and the vessel responds best when a relatively large vascular beds are involved rather than a small, capillary beds. Recently, the clinical efficacy of peripheral vasodilators have been challanged by many clinical investigators and clinicians. In this study, we have re-evaluated the efficacy of Ethaverine HCl as peripheral vasodilator in patients with vasospastic peripheral arterial disease. Ethaverine is claimed to be two to four times as potent a spasmolytic agent as papaverine in a variety of laboratory and clinical work.

• Journal of Chest Surgery
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• v.39 no.12 s.269
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• pp.913-919
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• 2006

Background: Vasodilatory shock has been implicated in life-threatening complications after open heart surgery, where the systemic inflammatory reaction is attributed to the cardiopulmonary bypass(CPB). The secretion of arginine vasopressin(AVP) has been found to be defective in a variety of vasodilatory shock states and administration of AVP markedly improves vasomotor tone and blood pressure. So we reviewed our experience of AVP therapy in patients with vasodilatory shock following heart surgery using CPB. Material and Method: From January 2004 to July 2006, we reviewed the records of patients who received AVP therapy for vasodilatory shock following heart surgery using CPB. Vasodilatory shock was defined as a mean arterial pressure lower(MAP) than 70 mmHg, a cardiac index greater than 2.5 $L/min/m^2$, peripheral vascular resistance lower than 800 $dyn/s/cm^5$, and vasopressor requirements. The hemodynamic responses of patients who received AVP therapy for vasodilatory shock after cardiac surgery were analyzed retrospectively. Result: One hundred ninety nine open cardiac surgery patients were consecutively included in this study. Twenty two patients(11.1%) met criteria for vasodilatory shock. Despite the administration of high dose catecholamine vasopressor, all patients were hypotensive with a mean arterial pressure less than 70 mmHg. AVP therapy increased MAP from $53.3{\pm}7.4\;to\;82.0{\pm}12.0$ mmHg at 1 hour (p<0.001) and decreased other vasopressor requirements from $25{\pm}7\;to\;18{\pm}6$ at 1 hour(p<0.001) and individually maintained it for 12 hours. Conclusion: Our date suggest that AVP may be a safe and an effective vasopressor in patients with vasodilatory shock. In patients exhibiting vasodilatory shock after heart surgery, replacement of AVP increases blood pressure and reduces catecholamine vasopressor requirements.

• Journal of Chest Surgery
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• v.39 no.1 s.258
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• pp.60-63
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• 2006

Vasodilatory shock has been implicated in life-threatening complications after cardiac surgery. This syndrome may result from the vasopressin deficiency following cardiopulmonary bypass (CPB), which do not respond to fluids or usual intravenous inotropes. We used arginine-vasopressin in adults with vasodilatory shock coming on cardiopulmonary bypass. Therefore, we report these cases with a review of articles.

• Journal of Chest Surgery
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• v.35 no.3
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• pp.227-230
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• 2002

The vasodilatory shock after cardiopulmonary bypass is defined as the condition involving severe and persistent form of hypotension, tachycardia, normal or increased cardiac output and decreased systemic vascular resistance. Because of the unsuccessful response to infusion of fluids or catecholamine vasopressors, a sustained systemic shock state occurs and results in a high morbidity and mortality. We successfully treated this syndrome of 3 patients after open heart surgery with low dose of arginine vasopressin(AVP). Therefore, we report these cases with a review of related articles.

• The Korean Journal of Pain
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• v.3 no.2
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• pp.144-148
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• 1990

정상인에서 Guanethidine Nicardipine Nitroglycerine Prostaglandin $E_1$을 피하주사하고 지속적인 복사열을 주사한 후에 Pain Meter NYT-5를 이용하여 동통역치를 측정하였다. 통증역치는 Guanethidine과 Nicardipine에 의해 상승되었으며 Nitroglycerine에 의해서는 거의 변화가 없고 Prostaglandin $E_1$에 의해서는 감소되었다. 이러한 변화는 지각신경섬유의 말단 감각수용체에 대한 감수성이 이들 혈관확장제에 대하여 서로 다른 작용을 나타내는것 같다.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1996.04a
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• pp.269-269
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• 1996

발모제에 관한 연구의 일환으로 현재 발모제로 쓰여지고 있는 미녹시딜에 구충제 또는 모근 혈관확장제 둥의 효능을 갖고 있는 씬나믹산을 반응시켜 새로운 화합물 (이하 CINMI라 칭함)을 만들었다. 이 화합물에 대하여 액성영향 및 반응시간 등 제반물성을 검토하고, 최적조건에서 흡광도를 측정하여 검량선을 작성하였으며, 그리고 결합구조 및 육모효과 등에 대하여 검토하였다.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1992.05a
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• pp.44-44
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• 1992

최근 $K^{＋}$ channel openers인 cromakalim과 Pinacidil이 새로운 종류의 혈관확장제로서 항고혈압 치료제로 소개되었다. 그러나 이들 약물의 이완 효과와 새포내 작용기전은 분명치 않다. 따라서 본 연구에서는 개의 관상 동맥에서 얻은 평활근 세포에서 $K^{＋}$ channel openers에 의한 이완의 세포내 기전을 규명하고자 시도하였다 혈관 평할근 세포(dispersed smooth muscle cells)를 collagenase를 이용한 효소소화(enzymatic digestion)에 의해 분리하고, saponin을 이용하여 permeabilize되게 하였다. frypan blue exclusion과 전자 현미경적 관찰에 의하여 세포의 viability를 확인하였다. Dispersed intact cells은 phenylephrine (PE)에 의하여 용량의존 수축반응을 보였고 ED$_{50}$는 2.3 $\times$ $10^{-12}$ M이었다. 이러한 PE에 의한 수축반응은 cromakalim과 pinacidil (ED$_{50}$, 1.2 $\times$ $10^{-12}$ M)의 용량에 의존하여 억제되었다.

• Journal of Chest Surgery
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• v.37 no.4
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• pp.364-368
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• 2004

Congenital pulmonary vein stenosis is a rare anomaly and related to high mortality due to progressive pulmonary hypertension and heart failure in infancy. Aggressive anti-failure medication and surgical treatment is recommended. Surgical options are balloon dilatation, endovascular stent, pneumonectomy, lung transplantation, patch grafting, and sutureless repair. We report a case of congenital pulmonary vein stenosis with normal anatomical connection successfully treated with sutureless technique and using pulmonary vasodilators, such as Sildenafil, lloprost and iNO postoperatively.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1993.04a
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• pp.85-85
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• 1993

뇌동맥계는 일과성 저혈압에 반응하여 혈관확장이 야기되고, 혈압 상승시에는 혈관수축이 일어남으로서 뇌혈류가 일정하게 조절된다. 이러한 자가조절은 뇌손상 등의 병적 상태에서 야기된다. 연구의 목적은 \circled1 Cromakalim, CGRP(calcitonin-gene related peptide), 및 substance P에 의하여 뇌연막동맥의 직경이 어떻게 변동하는가를 관찰하고 \circled2 이들 신경성 peptide의 작용에 대하여 $K^{＋}$ 통로 개방 봉쇄제인 glibenclamide의 전처치 효과를 검색하고 \circled3 Capsaicin 전처치가 뇌혈류 자가조절에 어떻게 영향을 미치는가를 검색하였다. 그 결과는 다음과 같다. 1. 뇌혈류 자가조절은 대퇴동맥을 통한 사혈에 의하여 혈압하강을 일으킬 때 뇌연막 동맥은 이완하였고, reservoir내의 혈액을 체내로 주입함로서 혈압반전을 일으켰을 때는 혈관 수축이 일어났다. 2. 연막동맥은 glibenclamide (1~3$\mu$M)의 관류에 의하여는 영향을 받아니하였다. 3. 혈압변동에 따른 혈관직경의 변화를 회기직선으로 분석하였다. Glibenclamide 1과 3$\mu$M의 전처치 관류에 의하여 혈압하강에 따른 혈관 이완경사도와 혈압반전에 따른 혈관수축 경사도가 대조군에 비하여 현저히 약화되었다. 4. Cromakalim (0.1-30$\mu$M)의 각 농도를 대뇌표면에 관류시 연막동맥의 기초직경은 약물농도에 의존하여 증가되었고, 이는 glibenclamide (1$\mu$M) 전처치 관류에 의하여 억제되었다. 5. CGRP (0.1~100 nM)와 substance P (0.1~10nM)도 용량에 의존하여 혈관이완을 일으켰다. 전자는 glibenclamide (1$\mu$M) 전처치 관류에 의하여 억제되었으나 후자는 영향을 받지 아니하였다. 6. Capsaicin(50 nmol: intracisternally) 주사에 의하여 뇌혈류자가조절의 변동이 초래되었다. 이상의 결과들을 종합하면 CGRP가 혈압변동에 의하여 반사적으로 유리되고, 이는 glibenclamide-sensitive $K^{＋}$ 통로에 작용하는 것으로 시사된다.

• Journal of Chest Surgery
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• v.32 no.1
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• pp.75-79
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• 1999

Budd-Chiari syndrome is a state of hepatic failure caused by impairment of blood flow anywhere from the inferior vena cava to the right atrium. In this case, a 45 year old patient had undergone membranotomy and dilatation with autogenous pericardial graft due to obstruction of the inferior vena cava caused by a congenital membrane in 1987. Ten years after the operation, restenosis occurred. Although a noninvasive method with a Gianturco stent dilatation was performed, a satisfactory result was not obtained. A reoperation was performed. The stenotic segment of inferior vena cava was excised and after augmentation with a prepared pentagon shaped Gore-Tex artificial graft allowing passage of two fingers. The patient's postoperative course was uneventful without signs of rebleeding or any other complications and the patient was discharged at postoperative two weeks without the use of anticoagulants. An excellent result was obtainable after operation using a prepared Gore-Tex graft and such a result. Reoperational case of Budd-Chiari syndrome may require rapid and excellent the operative techenic by prevention of massive bleeding under use of extracorporeal circulation.