ペースメーカー電位、歩調取り電位

WordNet

existing in possibility; "a potential problem"; "possible uses of nuclear power" (同)possible
the inherent capacity for coming into being (同)potentiality, potency
an implanted electronic device that takes over the function of the natural cardiac pacemaker (同)artificial_pacemaker
a specialized bit of heart tissue that controls the heartbeat (同)cardiac_pacemaker, sinoatrial_node, SA_node

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可能性のある,潜在的な / 可能性,潜在力 / 電位
(また《おもに米》『pacesetter』)ペースメーカー(レースで先頭に立って速度の調整役となる走者) / 脈拍調整器(心臓病の治療器)

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2016/05/25 07:32:58」(JST)

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In the pacemaking cells of the heart (e.g., the sinoatrial node), the pacemaker potential (also called the pacemaker current) is the slow, positive increase in voltage across the cell's membrane (the membrane potential) that occurs between the end of one action potential and the beginning of the next action potential. This increase in membrane potential is what causes the cell membrane, which typically maintains a resting membrane potential of -70 mV,^[1] to reach the threshold potential and consequently fire the next action potential; thus, the pacemaker potential is what drives the self-generated rhythmic firing (automaticity) of pacemaker cells, and the rate of change (i.e., the slope) of the pacemaker potential is what determines the timing of the next action potential and thus the intrinsic firing rate of the cell. In a healthy sinoatrial node (SAN, a complex tissue within the right atrium containing pacemaker cells that normally determine the intrinsic firing rate for the entire heart^[2]^[3]), the pacemaker potential is the main determinant of the heart rate. Because the pacemaker potential represents the non-contracting time between heart beats (diastole), it is also called the diastolic depolarization. The amount of net inward current required to move the cell membrane potential during the pacemaker phase is extremely small, in the order of few pAs, but this net flux arises from time to time changing contribution of several currents that flow with different voltage and time dependence. Evidence in support of the active presence of K⁺, Ca²⁺, Na⁺ channels and Na⁺/K⁺ exchanger during the pacemaker phase have been variously reported in the literature, but several indications point to the “funny”(I_f) current as one of the most important.^[4](see funny current). There is now substantial evidence that also sarcoplasmic reticulum (SR) Ca²⁺-transients participate to the generation of the diastolic depolarization via a process involving the Na–Ca exchanger.

Distinctions among autonomic foci

In reality, the heart has several pacemakers known as autonomic foci, each which fires at its own intrinsic rate:

SA node: 60–100 bpm
Atrial foci: 60–80 bpm
Junctional foci: 40–60 bpm
Ventricular foci: 20–40 bpm

The potentials will normally travel in order
SA node → atrial foci → junctional foci → ventricular foci

Pacemaker potentials are fired not only by SA node, but also by the other foci. However, the other firing frequencies are slower than the one of the SA node (as seen above). Normally, all the foci will end up firing at the SA node rate, not their intrinsic rate. The other foci attempt to fire at their intrinsic rate, but they are activated by the SA node before they can fire. This rapid firing causes all the foci to fire faster than their intrinsic rates, a phenomenon known as overdrive-suppression. Thus, in the normal, healthy heart, only the SA node intrinsic rate is observable.

Pathology

However, in pathological conditions, the intrinsic rate becomes apparent. Consider a heart attack which damages the region of the heart between the SA node and the atrial foci.

SA node → |block| atrial foci → junctional foci → ventricular foci

The other foci will not see the SA node firing; however, they will see the atrial foci. The heart will now beat at the intrinsic rate of the atrial foci.

Induction

The firing of the pacemaker cells is induced electrically by reaching the threshold potential of the cell membrane. The threshold potential is the potential an excitable cell membrane, such as a myocyte, must reach in order to induce an action potential.^[5] This depolarization is caused by very small net inward currents of calcium ions across the cell membrane, which gives rise to the action potential.^[6]^[7]

Bio-pacemakers

Bio-pacemakers are the outcome of a rapidly emerging field of research into a replacement for the electronic pacemaker. The bio-pacemaker turns quiescent myocardial cells (e.g. atrial cells) into pacemaker cells. This is achieved by making the cells express a gene which creates a pacemaker current.^[8]

References

^ Berne, Robert; Matthew Levy; Bruce Koeppen; Bruce Stanton (2004). Physiology. Elsevier Mosby. p. 276. ISBN 0-8243-0348-2.
^ Verkerk AO, van Boren MM, Peters RJ, Broekhuis E, Lam K, Coronel R, de Bakker JM, Tan HR (October 2007). "Pacemaker current (I)f)) in the human sinoatrial node". Eur Heart J 20 (1): 2472–8. doi:10.1093/eurheartj/ehm339. PMID 17823213.
^ Boron, Walter. F; Emile Boulpaep (2003). Medical Physiology. Elsevier Saunders. p. 489. ISBN 0-7216-0076-X.
^ DiFrancesco D (May 2006). "Funny channels in the control of cardiac rhythm and mode of action of selective blockers". Pharmacol. Res. 53 (5): 399–406. doi:10.1016/j.phrs.2006.03.006. PMID 16638640.
^ Campbell, Neil. A (1996). Biology. Benjamin Cummings. p. G–21. ISBN 0-07-366175-9.
^ Verkerk AO, van Ginneken AC, Wilders R, (January 2009). "Pacemaker activity of the human sinoatrial node: Role of the hyperpolarization-activated current, I(f).". Int J Cardiol 132 (3): 318–36. doi:10.1016/j.ijcard.2008.12.196. PMID 19181406.
^ Boron, Walter. F; Emile Boulpaep (2003). Medical Physiology. Elsevier Saunders. p. 487. ISBN 0-7216-0076-X.
^ Verkerk AO, Zegers JG, Van Ginneken AC, Wilders R (2008). "Dynamic action potential clamp as a powerful tool in the development of a gene-based bio-pacemaker". Conf Proc IEEE Eng Med Biol Soc 1: 133–6. doi:10.1109/IEMBS.2008.4649108. ISBN 978-1-4244-1814-5. PMID 19162611.

UpToDate Contents

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1. 心臓ペーシングのモード：名称および選択 modes of cardiac pacing nomenclature and selection
2. 一時的心臓ペーシング temporary cardiac pacing
3. ペーシングシステムの誤作動：評価およびマネージメント pacing system malfunction evaluation and management
4. 恒久的心臓ペースメーカー：適応 permanent cardiac pacing indications
5. 心不全における心臓ペーシングの概要 overview of cardiac pacing in heart failure

English Journal

Comparison of two valve systems for transapical aortic valve implantation: a propensity score-matched analysis†.

Kempfert J1, Meyer A2, Kim WK3, Van Linden A1, Arsalan M1, Blumenstein J4, Möllmann H4, Walther T1.
European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery.Eur J Cardiothorac Surg.2016 Feb;49(2):486-92. doi: 10.1093/ejcts/ezv042. Epub 2015 Feb 10.
OBJECTIVES: Several alternative transapical (TA) aortic prostheses for aortic valve implantation (AVI) have recently become available. Data directly comparing the performance of these different TA-AVI valves, however, are sparse. Therefore, we sought to analyse the performance of the better-establis
PMID 25669644

TRPC3 regulates the automaticity of embryonic stem cell-derived cardiomyocytes.

Qi Z1, Wong CK1, Suen CH1, Wang J2, Long C2, Sauer H3, Yao X4, Tsang SY5.
International journal of cardiology.Int J Cardiol.2016 Jan 15;203:169-81. doi: 10.1016/j.ijcard.2015.10.018. Epub 2015 Oct 9.
BACKGROUND: Cardiac pacemaking is a complex phenomenon that is not completely understood. Canonical transient receptor potential isoform 3 (TRPC3) channel is a cation channel that permeates both Ca(2+) and Na(+). TRPC3 was previously found to express in adult cardiomyocytes. However, its role in car
PMID 26512833

Left Ventricular Pacing Through Coronary Sinus is Feasible and Safe for Patients With Prior Tricuspid Valve Intervention.

Sideris S1, Drakopoulou M2, Oikonomopoulos G3, Gatzoulis K2, Stavropoulos G3, Limperiadis D3, Toutouzas K2, Tousoulis D2, Kallikazaros I1.
Pacing and clinical electrophysiology : PACE.Pacing Clin Electrophysiol.2016 Jan 14. doi: 10.1111/pace.12815. [Epub ahead of print]
BACKGROUND: In the presence of tricuspid valve intervention, right ventricular lead implantation is associated with the potential risk of tricuspid valve malfunction leading to a tricuspid regurgitation. Few cases have been reported with successful left ventricular pacing via the coronary sinus (CS)
PMID 26769172

Japanese Journal

Mucosal Immune Responses in W/W^v and SI/SI^d Mutant Mice

YOSHINO Naoto,KANNO Hiroyuki,TAKAHASHI Kiyomi [他],ENDO Masahiro,SATO Shigehiro
Experimental animals 61(4), 407-416, 2012-07-01
… In order to identify potential unanticipated side reactions and immune responses, the evaluation of candidate vaccines should include immunization of the murine model of the disease in question and mutant animals, as well as normal laboratory animals. … We employed WBB6F1-W/Wv and WBB6F1-Sl/Sld mutant mice, which are genetically mast cell deficient and lack intestinal pacemaker activity due to a severe deficiency in interstitial cells of Cajal. …
NAID 10030800432

Selective Sinoatrial Node Optical Mapping and the Mechanism of Sinus Rate Acceleration

SHINOHARA Tetsuji,PARK Hyung-Wook,JOUNG Boyoung,MARUYAMA Mitsunori,CHUA Su-Kiat,HAN Seongwook,SHEN Mark J.,CHEN Peng-Sheng,LIN Shien-Fong
Circulation journal : official journal of the Japanese Circulation Society 76(2), 309-316, 2012-01-25
… We simultaneously mapped intracellular Ca (Ca<sub>i</sub>) and membrane potential (V<sub>m</sub>) in 10 isolated, Langendorff-perfused normal canine RAs. … Isoproterenol (ISO, 0.03μmol/L) decreased the cycle length of the sinus beats, and shifted the leading pacemaker site from the middle or inferior SAN to the superior SAN in all RAs. …
NAID 10030035379