• Kosin Medical Journal
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• v.33 no.3
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• pp.396-401
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• 2018

Extraction of old pacemaker leads remains a complex procedure owing to fibrotic encapsulation and lead adhesions. We report a case of extraction of 15-year-old pacemaker leads by weight and pulley method. A 81-year-old man presented with exposed pacemaker leads out of body with purulent discharge from a pacemaker insertion site. He inserted DDD (dual chamber pacing, dual chamber sensing dual function) pacemaker implantation 15 years ago for SSS. Previously pacemaker battery was removed 3 years ago due to recurrent infection of pacemaker scar site. We extracted the pacemaker leads by weight and pulley method successfully without any complications.

• Journal of Chest Surgery
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• v.17 no.1
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• pp.125-128
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• 1984

The management of the exposed cardiac pacemaker or its lead is a new challenge to the plastic surgeon. This complication is not rare. Coburn et al. [1972] reported less than 5 percent, but Sowton et al. [1974] showed that over a period of 19 years, in a series of 372 patients, the pacing system had to be removed because of local wound breakdown or infection in 10 percent of the cases. The methods used to treat exposure may vary from removal and re-introduction at anterior site to the rotation of local flaps to cover the exposed pacemaker. Recently we have experienced 6 times of migration and recurrent skin ulcerations without pyogenic infection overlying the pacemaker in one patient. We developed a new technique, anchoring the pacemaker to the clavicle by a wire through the hole of clavicle and by creating a pocket under the pectoralis major muscle. Then we would like to emphasize this operating method could be choice of treatment to prevent the migration of pacemaker and the ulceration of skin when complication of implantation of pacemaker is occurred.

• Biomedical Science Letters
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• v.18 no.3
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• pp.218-226
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• 2012

Dopamine is an enteric neurotransmitter that regulates gastrointestinal motility. This study was done to investigate whether dopamine modulates spontaneous pacemaker activity in cultured interstitial cells of Cajal (ICCs) from mouse using whole cell patch clamp technique, RT-PCR and live $Ca^{2+}$ imaging analysis. ICCs generate pacemaker inward currents at a holding potential of -70 mV and generate pacemaker potentials in current-clamp mode. Dopamine did not change the frequency and amplitude of pacemaker activity in small intestinal ICCs. On the contrary dopamine reduced the frequency and amplitude of pacemaker activity in large intestinal ICCs. RT-PCR analysis revealed that Dopamine2 and 4-receptors are expressed in c-Kit positive ICCs. Dopamine2 and 4 receptor agonists inhibited pacemaker activity in large intestinal ICCs mimicked those of dopamine. Domperidone, dopamine2 receptor antagonist, increased the frequency of pacemaker activity of large intestinal ICCs. In $Ca^{2+}$-imaging, dopamine inhibited spontaneous intracellular $Ca^{2+}$ oscillations of ICCs. These results suggest that dopamine can regulate gastrointestinal motility through modulating pacemaker activity of large intestinal ICCs and dopamine effects on ICCs are mediated by dopamine2 receptor and intracellular $Ca^{2+}$ modulation.

• Journal of Chest Surgery
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• v.43 no.1
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• pp.86-88
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• 2010

Implanting a pacemaker is the most often used intervention for treating bradycardia. The most commonly used pacemaker is the intracardiac pacemaker, yet it can have many complications. An infected pacemaker can spread to systemic infection and the condition of the patient can quickly get worse, so if an infected pacemaker is suspected, then the pacemaker must be removed. Apart from the use of interventional methods such as a loop or a weight, we can take a more aggressive approach by using extracorporeal circulation for removal of the pacemaker. We report here on two cases in which extracorporeal circulation was used to remove the infected pacemakers.

• Molecules and Cells
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• v.42 no.6
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• pp.470-479
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• 2019

Interstitial cells of Cajal (ICCs) are pacemaker cells that exhibit periodic spontaneous depolarization in the gastrointestinal (GI) tract and generate pacemaker potentials. In this study, we investigated the effects of ghrelin and motilin on the pacemaker potentials of ICCs isolated from the mouse small intestine. Using the whole-cell patch-clamp configuration, we demonstrated that ghrelin depolarized pacemaker potentials of cultured ICCs in a dose-dependent manner. The ghrelin receptor antagonist [D-Lys] GHRP-6 completely inhibited this ghrelin-induced depolarization. Intracellular guanosine 5'-diphosphate-${\beta}$-S and pre-treatment with $Ca^{2+}$-free solution or thapsigargin also blocked the ghrelin-induced depolarization. To investigate the involvement of inositol triphosphate ($IP_3$), Rho kinase, and protein kinase C (PKC) in ghrelin-mediated pacemaker potential depolarization of ICCs, we used the $IP_3$ receptor inhibitors 2-aminoethoxydiphenyl borate and xestospongin C, the Rho kinase inhibitor Y-27632, and the PKC inhibitors staurosporine, Go6976, and rottlerin. All inhibitors except rottlerin blocked the ghrelin-induced pacemaker potential depolarization of ICCs. In addition, motilin depolarized the pacemaker potentials of ICCs in a similar dose-dependent manner as ghrelin, and this was also completely inhibited by [D-Lys] GHRP-6. These results suggest that ghrelin induced the pacemaker potential depolarization through the ghrelin receptor in a G protein-, $IP_3$-, Rho kinase-, and PKC-dependent manner via intracellular and extracellular $Ca^{2+}$ regulation. In addition, motilin was able to depolarize the pacemaker potentials of ICCs through the ghrelin receptor. Therefore, ghrelin and its receptor may modulate GI motility by acting on ICCs in the murine small intestine.

• Journal of Chest Surgery
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• v.48 no.2
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• pp.129-133
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• 2015

Severe and permanent tricuspid regurgitation induced by pacemaker leads is rarely reported in the literature. The mechanism of pacemaker-induced tricuspid regurgitation has been identified, but its management has not been well established. Furthermore, debate still exists regarding the proper surgical approach. We present the case of a patient with severe tricuspid regurgitation induced by a pacemaker lead, accompanied by triple valve disease. The patient underwent double valve replacement and tricuspid valve repair without removal of the pre-existing pacemaker lead. The operation was successful and the surgical procedure is discussed in detail.

• Proceedings of the KOSOMBE Conference
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• v.1998 no.11
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• pp.119-120
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• 1998

In this study, the design of the single-chamber pacemaker tester is presented. It is important to test the functions of the pacemaker before it is implanted into the patient. A pacemaker tester, that is presented in this study, is able to examine pacemaker parameters such as sensing threshold and refractory period. We need to make artificial intracardiac electrogram in order to test the pacemaker parameters. We know from the previous practical examples that a triangle pulse is similar to the physiologic intracardiac electrogram. The tester generates the simplified electrograms and PC software examines the output pulses of the pacemaker which is VVIR mode in closed-loop simulation.

• 전기의세계
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• v.23 no.5
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• pp.47-53
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• 1974

The electrical cardiac pacemaker model described in this paper simulates the most important functional properies of cardiac pacemaker cells. It is a minimum-parameter model which has a simple relaxation oscillator circuit as its main element. The electrical cardiac pacemaker model is analyzed in detail in order to show that its characteristic is similar to that of cardiac pacemaker cells. The main feature of the model is the possibility of controlling the time course phase 4 depolarization, the threshold level and the maximum level of repolarization, the rate of cardiac pacemaker. Emphasis is placed on phenomena of acceleration and frequency entrainment. This particular pacemaker model is very useful for the study of interactions between cardiac pacemakers and the description of the mechanism of arrhythmias.

• Journal of Life Science
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• v.31 no.7
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• pp.662-670
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• 2021

Interstitial cells of Cajal (ICCs) are the pacemaking cells in the gastrointestinal (GI) muscles that generate the rhythmic oscillation in membrane potentials known as slow waves. In the present study, we investigated the effects of mirtazapine, a noradrenergic and serotonergic antidepressant, on pacemaking potential in cultured ICCs from the murine small intestine. The whole-cell patch-clamp configuration was used to record pacemaker potential in cultured ICCs. Mirtazapine induced pacemaker potential depolarizations in a concentration-dependent manner in the current clamp mode. Y25130 (a 5-HT3 receptor antagonist), RS39604 (a 5-HT4 receptor antagonist), and SB269970 (a 5-HT7 receptor antagonist) had no effects on mirtazapine-induced pacemaker potential depolarizations. Also, methoctramine, a muscarinic M₂ receptor antagonist, had no effect on mirtazapine-induced pacemaker potential depolarizations, whereas 4-diphenylacetoxy-N-methyl-piperidine methiodide (4-DAMP), a muscarinic M₃ receptor antagonist, inhibited the depolarizations. When guanosine 5'-[β-thio] diphosphate (GDP-β-S; 1 mM) was in the pipette solution, mirtazapine-induced pacemaker potential depolarization was blocked. When an external Ca²⁺ free solution or thapsigargin, a Ca²⁺-ATPase inhibitor of the endoplasmic reticulum, was applied, the generation of pacemaker potentials disappeared, and under these conditions, mirtazapine induced pacemaker potential depolarizations. In addition, protein kinase C (PKC) inhibitor, calphostin C, and chelerythrine inhibited mirtazapine-induced pacemaker potential depolarizations. These results suggest that mirtazapine regulates pacemaker potentials through muscarinic M₃ receptor activation via a G protein-dependent and an external or internal Ca²⁺-independent PKC pathway in the ICCs. Therefore, mirtazapine can control GI motility through ICCs.

• Journal of Life Science
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• v.29 no.9
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• pp.1010-1015
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• 2019

The interstitial cells of Cajal (ICCs) are the pacemaker cells in the gastrointestinal (GI) tract. In the present study, the effects of olanzapine, an atypical antipsychotic agent, on pacemaker potentials in cultured ICCs from the small intestine of the mouse were investigated. The whole-cell patch-clamp configuration was used to record pacemaker potentials from cultured ICCs. Olanzapine produced pacemaker depolarizations in a concentration-dependent manner in current clamp mode. Methoctramine, a muscarinic $M_2$ receptor antagonist, did not inhibit olanzapine-induced pacemaker depolarizations, whereas 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP) muscarinic $M_3$ receptor antagonist did inhibit it. When guanosine 5'-[${\beta}$-thio] diphosphate (GDP-${\beta}$-S; 1 mM) was in the pipette solution, olanzapine-induced pacemaker depolarization was blocked. Also, low $Na^+$ solution externally eliminated the generation of pacemaker potentials and inhibited the olanzapine-induced pacemaker depolarizations. Additionally, the nonselective cation channel blocker, flufenamic acid, inhibited the olanzapine-induced pacemaker depolarizations. Pretreatment with U-73122, an active phospholipase C (PLC) inhibitor, also eliminated the generation of pacemaker potentials and suppressed the olanzapine-induced pacemaker depolarizations. These results suggested that olanzapine modulates the pacemaker potentials through muscarinic $M_3$ receptor activation by G protein-dependent external $Na^+$ and PLC pathway in the ICCs. Therefore, olanzapine could affect intestinal motility through ICCs.