• Proceedings of the PSK Conference
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• 2000.04a
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• pp.197.1-197.1
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• 2000

• Proceedings of the PSK Conference
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• 2001.04a
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• pp.242.1-242.1
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• 2001

• Proceedings of the PSK Conference
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• 2002.04a
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• pp.213.2-213.2
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• 2002

• Korean Journal of Clinical Pharmacy
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• v.16 no.2
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• pp.113-122
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• 2006

Purpose: A retrospective study was performed to assess the efficacy and tolerance of ${\beta}-blocker$ administration in patients with heart failure and diabetes. Method: Records of 164 patients who were treated for the heart failure condition more than a year were studied retrospectively. Patients were divided into 4 groups based on their diabetes(DM) status and the administration of ${\beta}-blockers$ ($DM+{\beta}-blocker$ group: 14, DM w/o ${\beta}-blocker$: 19, No DM + ${\beta}-blocker$: 62, No DM + no ${\beta}-blocker$: 69). All patients had been receiving conventional therapy such as digoxin, ACE-I, ARB, diuretics, nitrates, aspirin, anticoagulants or lipid-lowering agents. The primary endpoints (death and hospital admission) were recorded during 1 year period and hemodynamic factors (HR, LVEF, SBP, DBP) were obtained from all patient groups before and after 12 months of ${\beta}-blocker$ treatment. To evaluate toxicity of ${\beta}-blocker$, SCr, BUN, AST, ALT and Alkaline phosphatase were obtained. Result: There were less death and hospital admission in DM + ${\beta}-blocker$ group than in DM without ${\beta}-blocker$ group (p=0.014). Relative risk of hospital admission for $DM+{\beta}-blocker$ group over no DM group was 1.17. Long term ${\beta}-blocker$ administration was associated with an improvement of heart rate in patients with DM (P< 0.02) with no significant improvement of LVEF, SBP, DBP. in DM patient. In patient without DM, ${\beta}-blocker$ was associated with improvement in LVEF, HR and DBP (P<0.01, P<0.03), but not in SBP. The incidence of toxicity was similar between the four group with no significant difference. Conculsion: Treatment of heart failure patients with ${\beta}-blocker$ appears to be beneficial in terms of hospital admission event and several hemodynamic factors. The toxicities of ${\beta}-blocker$ treatment were not significant and the treatment is generally well-tolerated in most of the heart failure patients.

• The Korean Journal of Physiology and Pharmacology
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• v.6 no.1
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• pp.1-7
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• 2002

Congenital Long QT syndrome (LQTs) is a relatively rare pathologic disorder but results frequently in sudden cardiac death. Of the six LQTs that have been clinically described, five have been worked out for their genetic and biophysical profile. Most are generated by mutations which cause a loss of function in two delayed $K^+$ currents, $i_{Ks}\;and\;i_{Kr}.$ One syndrome is generated by mutations in the $Na^+$ channel which causes essentially a gain of function in the channel. Clinically the syndromes are characterized by slowed repolarization of the cardiac ventricular action potential and the occurrence of typical arrhythmias with undulating peaks in the electrocardiogram, called Torsade de Pointes. Arrhythmias are initiated by early or delayed afterdepolarizations and continue as reentry. Triggers for cardiac events are exercise (swimming; LQT1), emotion (arousal; LQT2) and rest/sleep (LQT3). ${\beta}-blockers$ have a high efficacy in the treatment of LQT1 and LQT2. In LQT3 their use is questionable. The study of congenital LQTsyndromes is a remarkable example of how basic and clinical science converge and take profit of each other's contribution.

• Journal of Chest Surgery
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• v.48 no.3
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• pp.220-224
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• 2015

A patient presented with loss of consciousness and conversion. During an exercise test, catecholaminergic polymorphic ventricular tachycardia (CPVT) resulted in cardiac arrest. He started taking medication (a beta-blocker and flecainide) and an implantable cardioverter defibrillator (ICD) was inserted, but the ventricular tachycardia did not resolve. Left cardiac sympathetic denervation (LCSD) was then performed under general anesthesia, and the patient was discharged on the second postoperative day without complications. One month after the operation, no shock had been administered by the ICD, and an exercise stress test did not induce ventricular tachycardia. Although beta- blockers are the gold standard of therapy in patients with CPVT, thoracoscopic LCSD is safe and can be an effective alternative treatment option for patients with intractable CPVT.

• The Korean Journal of Physiology
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• v.19 no.2
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• pp.101-111
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• 1985

Transient inward current (TI) was studied by the two micro-electrode voltage clamp technique in the sinoatrial node of the rabbit. The author confirmed that in $10^{-6}$ M ouabain TI was found in the SA node and investigated the effects of ions, $(Na^+,\;K^+,\;Ca^{2+})$, $\beta-agonist$ (isoprenaline), local anesthetics (quinidine, lidocaine) and Ca-blockers ($Co^{2+}$, verapamil, diltiazem) on the TI recorded during depolarizing voltage clamp pulses to -40 and -20 mV. The results obtained were as follows ; 1) $10^{-6}M$ ouabain increased the frequency of sinus action potential and decreased the amplitude, especially overshoot of action potential. TI was induced by the depolarizing voltage clamp Pulses and the magnitude of the slow inward current (isi) decreased and the time course was slowed by the same depolarizing pulses. 2) 30% $Na^{+}$ and 24mM $K^+$ decreased by $10^{-6}M$ ouabain and 6 mM $Ca^{2+}$ and $10^{-7}M$ isoprenaline increased TI, $i_{si}$ and current oscillations. 3) Quinidine $(5\times10^{-7}M)$ reduced TI and $i_{si}$ but lidocaine $(10^6\;-10^5M)$ didn't reduced or increase TI. Current oscillations increased and isi decreased by lidocaine. 4) Ca-blockers decreased the amplitude and the frequency of sinus action potential. TI and $i_{si}$ decreased significantly but were not abolished completely at the concentrations used in this experiment. Verapamil and diltiazem had inhibitory action on TI in $2\times10^{-7}M$ concentration and showed very slow recovery after wasting out with normal Tyrode solution.

• Journal of Gastric Cancer
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• v.13 no.3
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• pp.172-178
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• 2013

Purpose: The aims of this study were as follow: 1) to de scribe the expression status of estrogen receptor-${\alpha}$ and -${\beta}$ mRNAs in five gastric carcinoma cell lines; 2) to evaluate in vitro the effects of $17{\beta}$-estradiol and estrogen receptor antagonists on the proliferation of the cell lines. Materials and Methods: Detection of estrogen receptor-${\alpha}$ and estrogen receptor-${\beta}$ mRNA in five human gastric cancer cell lines (AGS, KATO III, MKN28, MKN45 and MKN74) was made by the reverse transcription-polymerase chain reaction system. To evaluate the effect of $17{\beta}$-estradiol and estrogen receptor antagonists on the proliferation of gastric cancer cell line, the cell lines which expressed both es trogen receptors were chosen and treated with $17{\beta}$-estradiol and estrogen receptor antagonists (methyl-piperidino-pyrazole and pyrazolo [1,5-a] pyrimidine). Cell proliferation was assessed with the methylthiazol tetrazolium test. Results: Estrogen receptor-${\alpha}$ and estrogen receptor-${\beta}$ mRNAs were expressed in three (KATO III, MKN28 and MKN45) and all of the five gastric cancer cell lines, respectively. At higher concentrations, $17{\beta}$-estradiol inhibited cell growth of MKN28, MKN45 and KATO III cell lines. Neither estrogen receptor-${\alpha}$ nor estrogen receptor-${\beta}$ antagonist blocked the anti-proliferative effect of $17{\beta}$-estradiol. Conclusions: Our results indicate that estrogen receptor-${\beta}$ mRNAs are preferentially expressed in gastric cancers and also imply that hormone therapy rather than estrogen receptor blockers may be a useful strategy for the treatment of estrogen receptor-${\beta}$ positive gastric cancer. Its therapeutic significance in gastric cancer are, however, limited until more evidence of the roles of estrogen receptors in the gastric cancer are accumulated.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.6
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• pp.753-761
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• 1998

Preconditioning of a heart with small doses of catecholamines induces a tolerance against the subsequent lethal ischemia. The present study was performed to find a specific receptor pathway involved with the catecholamine preconditioning and to test if adenosine plays a role in this cardioprotective effect. Isolated rat hearts, pretreated with small doses of ${\alpha}-\;or\;{\beta}-adrenergic$ agonists/antagonists, were subjected to 20 minutes ischemia and 20 minutes reperfusion by Langendorff perfusion method. Cardiac mechanical functions, lactate dehydrogenase and adenosine release from the hearts were measured before and after the drug treatments and ischemia. In another series of experiments, adenosine $A_1\;or\;A_2$ receptor blockers were treated prior to administration of adrenergic agonists. Pretreatments of a ${\beta}-agonist,\;isoproterenol(10^{-9}{\sim}10^{-7}\;M)$ markedly improved the post-ischemic mechanical function and reduced the lactate dehydrogenase release. Similar cardioprotective effect was observed with an ?-agonist, phenylephrine pretreatment, but much higher $concentration(10^{-4}\;M)$ was needed to achieve the same degree of cardioprotection. The cardioprotective effects of isoproterenol and phenylephrine pretreatments were blocked by a ${\beta}_1-adrenergic$ receptor antagonist, atenolol, but not by an ${\alpha}_1-antagonist,$ prazosin. Adenosine release from the heart was increased by isoproterenol, and the increase was also blocked by atenolol, but not by prazosin. A selective $A_1-adenosine$ receptor antagonist, 1,3-dipropyl-8-cyclopentyl xanthine (DPCPX) blocked the cardioprotection by isoproterenol pretreatment. These results suggest that catecholamine pretreatment protects rat myocardium against ischemia and reperfusion injury by mediation of ${\beta}_1-adrenergic$ receptor pathway, and that adenosine is involved in this cardioprotective effect.

• Journal of Yeungnam Medical Science
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• v.34 no.1
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• pp.128-131
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• 2017

Mid-ventricular obstruction (MVO) rarely occurs in patients without hypertrophic cardiomyopathy. Increased cardiac contractility may play an important role in causing MVO. We experienced a case of severe chest pain and MVO in a 50-year-old female patient. She had hypertension, diabetes, stroke and peripheral artery disease. Her blood pressure was very high (222/122 mmHg) with severe fluctuation. The transthoracic echocardiography revealed MVO accompanied by hyper-dynamic left ventricular systolic function. We regarded her chest pain and MVO as secondary findings related to other diseases. Coronary angiography and several tests for uncontrolled hypertension were performed, and those evaluations revealed that she had coronary artery disease and hyperthyroidism. We considered that the increase in the myocardial oxygen demand in response to the increase in cardiac contractility and workload associated with hyperthyroidism aggravated her symptoms and MVO. She was treated with methimazole and beta blockers and her symptoms dramatically improved.