• 고신대학교 의과대학 학술지
• /
• 제33권3호
• /
• pp.396-401
• /
• 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
• /
• 제17권1호
• /
• pp.125-128
• /
• 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.

• 대한의생명과학회지
• /
• 제18권3호
• /
• pp.218-226
• /
• 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
• /
• 제43권1호
• /
• pp.86-88
• /
• 2010

심박동기는 동기능 부전 증후군에서부터 완전 방실차단까지 서맥의 치료에 가장 보편적으로 사용되는 중재적 치료다. 일반적으로 경정맥을 통한 심내 심박동기를 많이 사용하고 있으나 감염 및 혈전증, 박동기의 기능부전, 부정맥, 심근천공, 삼첨판 폐쇄부전증 등의 합병증이 발생할 수 있다. 심박동기의 감염은 전신감염으로 이행되어 환자 상태가 빠르게 악화될 수 있으므로 감염으로 의심되면 제거하는 것이 원칙이다. 추나 올가미 등을 이용한 방법등 비수술적인 방법외에도 체외순환을 이용한 적극적인 제거도 환자 상태에 따라 고려해야 할 것이다. 감염된 심박동기를 체외순환을 이용하여 제거한 두 개의 증례를 보고하는 바이다.

• Molecules and Cells
• /
• 제42권6호
• /
• pp.470-479
• /
• 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
• /
• 제48권2호
• /
• pp.129-133
• /
• 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.

• 대한의용생체공학회:학술대회논문집
• /
• 대한의용생체공학회 1998년도 추계학술대회
• /
• pp.119-120
• /
• 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
• /
• 제23권5호
• /
• pp.47-53
• /
• 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.

• 생명과학회지
• /
• 제31권7호
• /
• pp.662-670
• /
• 2021

카할세포는 위장관 근육의 pacemaker 세포이다. 이번 연구는 생쥐 소장에서 얻은 카할세포를 배양하여 노르아드레날린성 및 세로토닌성 항우울제인 미르타자핀의 효과를 조사했다. 전기생리학적인 방법을 이용하여 카할세포의 pacemaker potential의 변화를 측정하였다. 미르타자핀은 농도 의존적 방식으로 카할세포 탈분극을 일으켰다. Y25130 (5-HT3 수용체 길항제), RS39604 (5-HT4 수용체 길항제) 또는 SB269970 (5-HT7 수용체 길항제)은 미르타자핀에 의한 카할세포 탈분극에 영향을 미치지 않았다. 또한, 무스카린성 M2 수용체 길항제인 메톡 트라민은 미르타자핀에 의한 카할세포의 탈분극에 영향을 미치지 않은 반면, 무스카린성 M3 수용체 길항제인 4-DAMP는 카할세포의 탈분극을 억제하였다. GDP-β-S를 피펫을 통해 카할세포내로 넣었을 때, 미르타자핀에 카할세포 탈분극이 억제되었다. 외부에 칼슘이 없는 용액 또는 소포체의 Ca²⁺-ATPase 억제제인 thapsigargin이 있는 경우 미르타자핀에 의한 카할세포 탈분극이 나타났다. 또한, protein kinase C (PKC) 억제제인 칼포스틴 C 또는 chelerythrine은 미르타자핀에 의한 탈분극을 억제했습니다. 이러한 결과는 미르 타자핀이 카할세포에서 G 단백질 및 PKC 경로에 의한 무스카린성 M3 수용체 활성화를 통해 탈분극을 조절 함을 알 수 있다. 따라서 미르타자핀이 카할세포를 통해 위장관 운동성을 조절할 수 있음을 시사한다.

• 생명과학회지
• /
• 제29권9호
• /
• pp.1010-1015
• /
• 2019

카할세포는 위장관에서 향도잡이 역할을 한다. 본연구에서는 생쥐 소장 카할세포에서 발생되는 향도잡이 기능에서 올란자핀의 역할을 연구하였다. 패치클램프 방법을 사용하여 향도잡이 전압을 측정하였다. 올란자핀에 의해서 카할세포 향도잡이 전압이 탈분극 되었으며, 이 탈분극은 무스카린성 3번 수용체 억제제에 의해서 억제 되었다. 세포내 $GDP{\beta}S$을 넣어주니 올란자핀에 의해 향도잡이 전압 탈분극이 억제되었다. 또한, 세포밖 $Na^+$ 농도 감소와 비선택성 양이온 통로 억제제에 의해서 올란자핀에 의한 향도잡이 전압 탈분극이 억제 되었다. 세포내 PLC기전의 억제제인 U-73122에 의해서 올란자핀에 의한 향도잡이 전압 탈분극이 억제 되었다. 이러한 결과로 올란자핀은 무스카린성 3번 수용체를 통해서 세포내 G 단백질과 PLC기전 및 세포밖 $Na^+$이 관여함을 알 수 있었다. 따라서 올란자핀은 카할세포를 통해서 장운동성을 조절 할 수 있을 것으로 생각된다.