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Electrical Properties of the Heart
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Cardiac pacemaker cells generate the inherent automaticity and rhythmicity of the heart; the ionic basis of pacemaker potentials was described in the section ‘Electrophysiological features of the sinoatrial node’. The SA node, other atrial centres, the AV node and the bundle of His all have inherent pacemaker activity, but the SA node is the most active and suppresses the others. The cardiac action potential generated by the SA node spreads directly through atrial muscle by gap junctions between adjacent fibres, producing simultaneous contraction of both atria. There is no direct electrical connection between atrial and ventricular muscles, and the cardiac action potential reaches the ventricles through the AV node and then the bundle of His. AV node transmission is associated with a delay of 0.1 s, which allows the atria to finish filling the ventricles before they contract.
Special Measurement Techniques
Published in Sujoy K. Guba, Bioengineering in Reproductive Medicine, 2020
Electrical activity can be monitored with extracellular electrodes from multiple sites along the tube at a time. It has been seen that when electrical activity commences at one site the activity travels in both abovarian and adovarian directions as evidenced by the sequential time lag in the oscillations picked up by the electrodes at distances away from the site of initial generation of the activity. These locations of initiation of electrical activity have been termed as “pacemakers” and the surface electrode technique is adequate to pick up the pacemaker potentials.
Role of Cell-to-Cell Coupling in Control of Myometrial Contractility and Labor
Published in Robert E. Garfield, Thomas N. Tabb, Control of Uterine Contractility, 2019
It has been proposed that any muscle cell can act as a pacemaker cell and it has been shown that nonpacemaker regions can become pacemakers by the application of oxytocin, acetylcholine, or prostaglandins but not by simply depolarizing the membrane with high K solutions.55 Stretching of the uterine wall also induces pacemaker activity. Pacemaker potentials are independent of nerve activity, because nerve blocking agents fail to prevent them. However, neuronal or hormonal influences may modulate the activity of the pacemaker cells and induce activity and impose directionality.
Prokinetic effects of Citrus reticulata and Citrus aurantium extract with/without Bupleurum chinense using multistress-induced delayed gastric emptying models
Published in Pharmaceutical Biology, 2023
Yanrong Gong, Xiaoxia Liang, Yanting Dai, Xiang Huang, Qiaozhen Su, Yan Ma, Fenglian Chen, Shuling Wang
Interstitial cells of Cajal are derived from mesenchymal precursor cells that express c-kit, a receptor for stem cell ligand. Therefore, ICC can be identified with c-kit immunoreactivity. ICC associated with the myenteric plexus generate pacemaker activity in the form of slowly propagating waves of depolarization that provide rhythmicity and the direction of propagation to the slow-wave-driven motor patterns of the small intestine (Huizinga and Parsons 2019). Lack of normal pacemaker activity generated by ICC could account for symptoms of intestinal obstruction in the absence of mechanical obstruction. A considerable body of evidence has revealed that intracellular Ca2+ oscillations in ICC periodically activate plasmalemmal Ca2+-dependent ion channels and thereby generate pacemaker potentials (Streutker 2003). Our study showed both AuCiBup and AuCi increased ICC numbers and extracellular Ca2+ influx which might act as the underlying mechanism of their prokinetic activity. Anoctamin-1 (ANO1), the most studied member of anoctamin family of calcium-activated chloride channels, is a prominent conductance in ICC and these channels appear to be involved in pacemaker activity and in responses to enteric excitatory neurotransmitters (Sanders 2012). It is reported that melastatin-type transient receptor potential channel 7 (TRPM7) is required for intestinal pacemaking activity (Kim 2005). Whether the prokinetic effects of AuCiBup and AuCi are associated with ANO1 or TRPM7 is still in further research.
Biological therapies targeting arrhythmias: are cells and genes the answer?
Published in Expert Opinion on Biological Therapy, 2018
Debbie Falconer, Nikolaos Papageorgiou, Emmanuel Androulakis, Yasmin Alfallouji, Wei Yao Lim, Rui Providencia, Dimitris Tousoulis
Proof of concept has been provided using a variety of approaches to increased inward current or decreased repolarizing current as a basis for propagation of a pacemaker potential [6]. In this arena of research, both embryonic stem cells (ESCs) and human mesenchymal stem cells (hMSCs) have been the main area of focus, although other cell sources (skeletal myoblasts; fibroblasts; cardiac stem cells) have been utilized. Both need electrical integration into host myocardium to allow for initiation of pacemaker activity, but this does not involve further engineering because both successfully form functional gap junctions with adjacent myocytes due to abundant connexin expression [27].