scholarly journals Dynamics of action potential head-tail interaction during reentry in cardiac tissue: ionic mechanisms

2000 ◽  
Vol 279 (4) ◽  
pp. H1869-H1879 ◽  
Author(s):  
Thomas J. Hund ◽  
Niels F. Otani ◽  
Yoram Rudy
Keyword(s):  
Action Potential ◽  
Wave Front ◽  
Cardiac Tissue ◽  
Excitation Wave ◽  
One Dimensional ◽  
Spatial Oscillations ◽  
Ionic Mechanisms ◽  
High Degree ◽  
Dynamics Of Action ◽  
Transient Oscillations

In a sufficiently short reentry pathway, the excitation wave front (head) propagates into tissue that is partially refractory (tail) from the previous action potential (AP). We incorporate a detailed mathematical model of the ventricular myocyte into a one-dimensional closed pathway to investigate the effects of head-tail interaction and ion accumulation on the dynamics of reentry. The results were the following: 1) a high degree of head-tail interaction produces oscillations in several AP properties; 2) Ca2+-transient oscillations are in phase with AP duration oscillations and are often of greater magnitude; 3) as the wave front propagates around the pathway, AP properties undergo periodic spatial oscillations that produce complicated temporal oscillations at a single site; 4) depending on the degree of head-tail interaction, intracellular [Na+] accumulation during reentry either stabilizes or destabilizes reentry; and 5) elevated extracellular [K+] destabilizes reentry by prolonging the tail of postrepolarization refractoriness.

Understanding the electrical behavior of the action potential in terms of elementary electrical sources

2015 ◽  
Vol 39 (1) ◽  
pp. 15-26 ◽  
Author(s):  
Javier Rodriguez-Falces
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Present Report ◽  
Electrical Potential ◽  
Ionic Currents ◽  
New Approach ◽  
Electrical Potentials ◽  
Proposed Model ◽  
Ionic Mechanisms ◽  
Human Electrophysiology

A concept of major importance in human electrophysiology studies is the process by which activation of an excitable cell results in a rapid rise and fall of the electrical membrane potential, the so-called action potential. Hodgkin and Huxley proposed a model to explain the ionic mechanisms underlying the formation of action potentials. However, this model is unsuitably complex for teaching purposes. In addition, the Hodgkin and Huxley approach describes the shape of the action potential only in terms of ionic currents, i.e., it is unable to explain the electrical significance of the action potential or describe the electrical field arising from this source using basic concepts of electromagnetic theory. The goal of the present report was to propose a new model to describe the electrical behaviour of the action potential in terms of elementary electrical sources (in particular, dipoles). The efficacy of this model was tested through a closed-book written exam. The proposed model increased the ability of students to appreciate the distributed character of the action potential and also to recognize that this source spreads out along the fiber as function of space. In addition, the new approach allowed students to realize that the amplitude and sign of the extracellular electrical potential arising from the action potential are determined by the spatial derivative of this intracellular source. The proposed model, which incorporates intuitive graphical representations, has improved students' understanding of the electrical potentials generated by bioelectrical sources and has heightened their interest in bioelectricity.

Effects of Na+ and K+ channel blockade on vulnerability to and termination of fibrillation in simulated normal cardiac tissue

2005 ◽  
Vol 289 (4) ◽  
pp. H1692-H1701 ◽  
Author(s):  
Zhilin Qu ◽  
James N. Weiss
Keyword(s):  
Action Potential ◽  
Cardiac Tissue ◽  
Theoretical Perspective ◽  
Conduction Block ◽  
Dynamical Instability ◽  
K Channel ◽  
Channel Blockade ◽  
Wave Instability ◽  
Transient Time ◽  
Underlying Mechanisms

Na+ and K+ channel-blocking drugs have anti- and proarrhythmic effects. Their effects during fibrillation, however, remain poorly understood. We used computer simulation of a two-dimensional (2-D) structurally normal tissue model with phase I of the Luo-Rudy action potential model to study the effects of Na+ and K+ channel blockade on vulnerability to and termination of reentry in simulated multiple-wavelet and mother rotor fibrillation. Our main findings are as follows: 1) Na+ channel blockade decreased, whereas K+ channel blockade increased, the vulnerable window of reentry in heterogeneous 2-D tissue because of opposing effects on dynamical wave instability. 2) Na+ channel blockade increased the cycle length of reentry more than it increased refractoriness. In multiple-wavelet fibrillation, Na+ channel blockade first increased and then decreased the average duration or transient time (<Ts>) of fibrillation. In mother rotor fibrillation, Na+ channel blockade caused peripheral fibrillatory conduction block to resolve and the mother rotor to drift, leading to self-termination or sustained tachycardia. 3) K+ channel blockade increased dynamical instability by steepening action potential duration restitution. In multiple-wavelet fibrillation, this effect shortened <Ts> because of enhanced wave instability. In mother rotor fibrillation, this effect converted mother rotor fibrillation to multiple-wavelet fibrillation, which then could self-terminate. Our findings help illuminate, from a theoretical perspective, the possible underlying mechanisms of termination of different types of fibrillation by antiarrhythmic drugs.

ROLE OF ACTION POTENTIAL SHORTENING IN THE PREVENTION OF ARRHYTHMIAS IN CANINE CARDIAC TISSUE

1999 ◽  
Vol 26 (12) ◽  
pp. 964-969 ◽  
Author(s):  
Kawonia P Mull ◽  
Qadriyyah Debnam ◽  
Syeda M Kabir ◽  
Mohit Lal Bhattacharyya
Keyword(s):  
Action Potential ◽  
Cardiac Tissue ◽  
Action Potential Shortening

Enhanced myocyte-based biosensing of the blood-borne signals regulating chronotropy

2002 ◽  
Vol 92 (2) ◽  
pp. 581-585 ◽  
Author(s):  
Jay M. Edelberg ◽  
Jason T. Jacobson ◽  
David S. Gidseg ◽  
Lilong Tang ◽  
David J. Christini
Keyword(s):  
Cardiac Myocyte ◽  
Cardiac Tissue ◽  
Critical Role ◽  
Excitable Tissue ◽  
Time Determination ◽  
Molecular Plasticity ◽  
Relationship Of ◽  
High Degree

Biosensors play a critical role in the real-time determination of relevant functional physiological needs. However, typical in vivo biosensors only approximate endogenous function via the measurement of surrogate signals and, therefore, may often lack a high degree of dynamic fidelity with physiological requirements. To overcome this limitation, we have developed an excitable tissue-based implantable biosensor approach, which exploits the inherent electropotential input-output relationship of cardiac myocytes to measure the physiological regulatory inputs of chronotropic demand via the detection of blood-borne signals. In this study, we report the improvement of this application through the modulation of host-biosensor communication via the enhancement of vascularization of chronotropic complexes in mice. Moreover, in an effort to further improve translational applicability as well as molecular plasticity, we have advanced this approach by employing stem cell-derived cardiac myocyte aggregates in place of whole cardiac tissue. Overall, these studies demonstrate the potential of biologically based biosensors to predict endogenous physiological dynamics and may facilitate the translation of this approach for in vivo monitoring.

Modeling of IK1 mutations in human left ventricular myocytes and tissue

2007 ◽  
Vol 292 (1) ◽  
pp. H549-H559 ◽  
Author(s):  
Gunnar Seemann ◽  
Frank B. Sachse ◽  
Daniel L. Weiss ◽  
Louis J. Ptáček ◽  
Martin Tristani-Firouzi
Keyword(s):  
Action Potential ◽  
Cardiac Tissue ◽  
Ventricular Myocytes ◽  
Torsade De Pointes ◽  
Low Frequency ◽  
Mechanistic Explanation ◽  
Left Ventricular ◽  
Autosomal Dominant Disorder ◽  
Modeling Approach ◽  
Dispersion Of Repolarization

Elucidation of the cellular basis of arrhythmias in ion channelopathy disorders is complicated by the inherent difficulties in studying human cardiac tissue. Thus we used a computer modeling approach to study the mechanisms of cellular dysfunction induced by mutations in inward rectifier potassium channel (Kir)2.1 that cause Andersen-Tawil syndrome (ATS). ATS is an autosomal dominant disorder associated with ventricular arrhythmias that uncommonly degenerate into the lethal arrhythmia torsade de pointes. We simulated the cellular and tissue effects of a potent disease-causing mutation D71V Kir2.1 with mathematical models of human ventricular myocytes and a bidomain model of transmural conduction. The D71V Kir2.1 mutation caused significant action potential duration prolongation in subendocardial, midmyocardial, and subepicardial myocytes but did not significantly increase transmural dispersion of repolarization. Simulations of the D71V mutation at shorter cycle lengths induced stable action potential alternans in midmyocardial, but not subendocardial or subepicardial cells. The action potential alternans was manifested as an abbreviated QRS complex in the transmural ECG, the result of action potential propagation failure in the midmyocardial tissue. In addition, our simulations of D71V mutation recapitulate several key ECG features of ATS, including QT prolongation, T-wave flattening, and QRS widening. Thus our modeling approach faithfully recapitulates several features of ATS and provides a mechanistic explanation for the low frequency of torsade de pointes arrhythmia in ATS.

scholarly journals How Hyperpolarization and the Recovery of Excitability Affect Propagation through a Virtual Anode in the Heart

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Nicholas P. Charteris ◽  
Bradley J. Roth
Keyword(s):  
Wave Front ◽  
Time Constant ◽  
Computer Model ◽  
Propagation Speed ◽  
One Dimensional ◽  
Upper Limit ◽  
Rapid Propagation ◽  
Upper Limit Of Vulnerability ◽  
Key Factor ◽  
Sodium Inactivation

Researchers have suggested that the fate of a shock-induced wave front at the edge of a “virtual anode” (a region hyperpolarized by the shock) is a key factor determining success or failure during defibrillation of the heart. In this paper, we use a simple one-dimensional computer model to examine propagation speed through a hyperpolarized region. Our goal is to test the hypothesis that rapid propagation through a virtual anode can cause failure of propagation at the edge of the virtual anode. The calculations support this hypothesis and suggest that the time constant of the sodium inactivation gate is an important parameter. These results may be significant in understanding the mechanism of the upper limit of vulnerability.

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