• Journal of Chest Surgery
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• v.18 no.1
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• pp.1-6
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• 1985

Isolated sinus node cells of the rabbit were used to assess the effects of extracellular Na, K, Ca and Mg concentrations on cardiac pacemaker activity. With intracellular glass micro-electrodes spontaneous action potentials of SA node were recorded and the effects of various ions and their blockers were analyzed in terms of the cycle length, the amplitude and the duration of action potentials, the results obtained were as follows. 1. Sodium reduction [up to 30%] decreased the amplitude of action potential and lengthened the cycle length. TTX, specific blocker of Na channel slightly lengthened the cycle length. 2. Increasing potassium ion concentration, the duration of action potential decreased and the frequency increased in 6mM, however, spontaneous action potential was stopped in 24 mM. Barium ion known to be decreasing K conductance increased the duration of action potential but no significant change in the cycle length was noticed. 3. Calcium ion has shortening effect on the duration and the cycle length of action potential but not with dose-dependent manner. Cadmium ion .[0.02mM] lengthened cycle length and the duration of action potential. 4. Increasing the concentration of magnesium ion the cycle length was lengthened, significantly.

• BMB Reports
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• v.48 no.12
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• pp.677-684
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• 2015

Cardiovascular function is regulated by the rhythmicity of circadian, infradian and ultradian clocks. Specific time scales of different cell types drive their functions: circadian gene regulation at hours scale, activation-inactivation cycles of ion channels at millisecond scales, the heart's beating rate at hundreds of millisecond scales, and low frequency autonomic signaling at cycles of tens of seconds. Heart rate and rhythm are modulated by a hierarchical clock system: autonomic signaling from the brain releases neurotransmitters from the vagus and sympathetic nerves to the heart's pacemaker cells and activate receptors on the cell. These receptors activating ultradian clock functions embedded within pacemaker cells include sarcoplasmic reticulum rhythmic spontaneous Ca²⁺ cycling, rhythmic ion channel current activation and inactivation, and rhythmic oscillatory mitochondria ATP production. Here we summarize the evidence that intrinsic pacemaker cell mechanisms are the end effector of the hierarchical brain-heart circadian clock system.

• Journal of Chest Surgery
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• v.28 no.2
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• pp.177-179
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• 1995

Sinus venosus type atrial septal defect is commonly associated with partial anomalous pulmonary venous return[PAPVR . Ideal surgical repair of sinus venosus ASD with PAPVR demands complete closure of septal defect with redirection of the anomalous pulmonary venous return to the left atrium without obstructing the superior vena cava[SVC or the anomalous pulmonary vein and without injury of sinoatrial node and residual shunt. In our two patients, the closure of sinus venosus ASD and correction of PAPVR could be accomplished by simple direct sutures without using a patch or flap. Both patients had a good outcome.

• Clinical and Experimental Pediatrics
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• v.46 no.2
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• pp.195-197
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• 2003

Sick sinus syndrome(SSS) constitutes a spectrum of cardiac arrhythmia, including sinus bradycardia, sinus pause-arrest, sinoatrial block, slow escape rhythm, bradyarrhythmia and tachyarrhythmia. SSS is relatively uncommon in children but its exact incidence is unknown because diagnostic criteria are not uniform and most children with SSS, in general are asymptomatic. SSS may be primary(organic sinus node disease) or secondary(cardiac surgery comprises much of SSS in children and adolescents), but it can hardly be caused by familial relations as well. We reports an occurrence of familial sick sinus syndrome. Mother was diagnosed as SSS, which was presented by symptoms of dizziness and treated by permanent pacemaker(DDD). Also, two daughters revealed SSS with non-compacted cardiomyopathy on neonatal screening and fetal echocardiography respectively. We concluded that familial SSS may occur, so familial screening should be suggested.

• Korean Journal of Veterinary Research
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• v.41 no.3
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• pp.311-317
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• 2001

In this work we have investigated the physiological effects of $MgCl_2$ in isolated atrium, papillary muscle, perfused heart and anesthesized guinea pig, The addition or infusion of $MgCl_2$ (0~20 mM or mg/kg) to perfused hearts and to anesthesized guinea pigs induced a marked and dose-dependent negative chronotropic effect. The sinoatrial node automaticity could also be reduced by $MgCl_2$. The addition of $MgCl_2$to isolated atria and to papillary muscles induced a marked and dose-dependent negative inotropic effect. The threshold voltage could be increased by $MgCl_2$in papillary muscle. Increasing $MgCl_2$ shortened the action potential duration (APD) in dose-dependent manner at 30% ($APD_{30}$) and 90% repolarization ($APD_{90}$) measured with conventional microelectrode technique in papillary muscle. In anesthesized guinea pig, the magnesium infusion resulted in a dose-dependent drop in blood pressure. These results suggested that magnesium is closely associated with cardiac physiological condition and exerts antiarrhythmic activities.

• Proceedings of the Korean Biophysical Society Conference
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• 2003.06a
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• pp.19-19
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• 2003

We have developed a cardiac cell model (Kyoto Model) for the sinoatrial node and ventricle, which is composed of a common set of kinetic equations of membrane ionic currents, Ca$\^$2+/dynamics of sarcoplasmic reticulum and contractile protein. To expand this model by including metabolic pathways, the intracellular ATP metabolism, which is pivotal in cardiac excitation - contraction coupling, was incorporated. ATP consumption by the sarcolemmal Na$\^$+/ pump and the Ca pump in the sarcoplasmic reticulum were calculated with stoichiometry of 3Na:2K:1ATP and 2Ca:1ATP, respectively. ATP consumption by contraction was estimated according to experimental data. Dependence of contraction on ATP and inorganic phosphate was modeled, based on data of skinned cardiac fiber. in production by mitochondrial oxidative phosphorylation was modified from Korzeniewski '||'&'||' Zoladz (2001), and creatine kinase and adenylate kinase reactions were incorporated. ATP dependence of ATP-sensitive K channel and L type Ca channel were also included.

• The Korean Journal of Physiology
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• v.20 no.1
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• pp.17-29
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• 1986

The present study was carried out to observe the effect of triiodothyronine on heart, one of the target organ of thyroid hormone. There are many reports that tachycardia, arrythmia, and agumentation of sodium, potassium pump activity are caused in hyperthyroid animal. To examine these cardiac positive chronotropic effects on sinoatrial (SA) node and atrial muscle, hyperthyroid state was induced experimentally by the injecion of 3,3',5-1-triiodothyronine $(T_3)$ in $3{\sim}6$ month-old rabbits. Then intracellular recordings by inserting glass microelectrode into cell were obtained in SA node and atrial muscle. The results can be summarized as follows : 1) Heartbeat was increased from $169.6{\pm}28.0\;to\;264.2{\pm}18.0$ beats per minute, while body weight was decreased to 68f of the initial body weight (Day 1). 2) In experimental group, the duration of action potential at 80% repolarization was decreased from $148.0{\pm}29.1\;to\;107{\pm}13.6msec$. This suggested the increase heartbeat. 3) The firing rate in hyperthyroid group markedly reduced under the 15 mM potassium Tyrode (p<0.005). 4) In hyperthyroid group, depolarization of atrial muscle cell was lowered significantly in 15 mM (p<0.05), 20 mM (p<0.05) potassium Tyrode solution. 5) Sodium-potassium pump activities in experimental group were higher than those in control group in both SA node (p<0. 1) and atrial muscle (p<0.025). 6) In lower concentration of $MnCl_2$, the excitability of SA node in hyperthyroid group was decreased more than that in control group. Effective inhibitory dose $(ID_{50})$ as 0.6 mM in hyperthyroid statd and 1.1 mM in control group.

• Neonatal Medicine
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• v.18 no.2
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• pp.395-398
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• 2011

Sick sinus syndrome (SSS) is a disorder characterized by sinus node dysfunction. Although the condition is most common in the elderly, it can occur in children including neonates and its recognition and treatment are important. The diagnosis of SSS is based on the presence of sinus bradycardia, sinus arrest or exit block, combinations of sinoatrial and atrioventricular nodal conduction disturbances, and atrial tachyarrhythmias documented in the Holter recordings. In most children with SSS, previous history of congenital heart malformation or cardiac surgery is noted. SSS is also seen in the children including neonates without heart disease or other contributing factors, however SSS is most often idiopathic. The treatment of SSS depends on the basic rhythm problem, but generally involves the placement of a cardiac pacemaker. We report a case of SSS in extremely low birth weight infant without congenital heart disease and suggest that the treatment system is necessary for preterm infants with SSS.