Analysis of field-induced transmembrane potential responses of single cardiac cells in terms of active and passive components

2002 ◽  
Author(s):  
V. Sharma ◽  
Leslie Tung
Keyword(s):  
Transmembrane Potential ◽  
Cardiac Cells ◽  
Passive Components

Intracellular calcium and electrogram in ischemic isolated rat heart

1980 ◽  
Vol 239 (3) ◽  
pp. H380-H390
Author(s):  
P. Carbonin ◽  
M. Di Gennaro ◽  
R. Valle ◽  
R. Beranbei ◽  
A. Habed
Keyword(s):  
Rat Heart ◽  
Transmembrane Potential ◽  
Isolated Rat Heart ◽  
Cardiac Cells ◽  
Free Medium ◽  
Activation Time ◽  
Intraventricular Conduction ◽  
Myocardial Area ◽  
Variation Rate ◽  
Isolated Rat

The electrogram (EG) of the isolated rat heart during ischemic or anoxic perfusion has been studied. Reduction of the coronary flow rate (CFR) induced an increase of voltage (V) both in unipolar epicardial EG and in transmural bipolar EG. The V increase did not occur during anoxic perfusin. The ischemic increase cannot be due to a disturbance in the His-Purkinje or intraventricular conduction because it was observed also in the circumscribed myocardial area, which was explored by means of the transmural bipolar EG. Likewise it cannot be due to an intramural block because it occurs before one observes an augmentation of epicardial activation time or a decrease of dV/dtmax. Therefore, the ischemic V increase should be due to a modification of transmembrane potential. The variation rate of V, of dP/dt, and of myocardial ATP behaved in a similar way during underperfusion. Varying intracellular Ca2+ by means of a Ca2+-free medium or verapamil reduces the ischemic V increase. The dynamics of the ischemic V increase may be represented in order of succession by: inhibition of oxidative metabolism, augmentation of intracellular Ca2+, increase of K+ conductance, and hyperpolarization of cardiac cells.

DERIVING AN ELECTRIC CIRCUIT EQUIVALENT MODEL OF CELL MEMBRANE PORES IN ELECTROPORATION

2013 ◽  
Vol 08 (01n02) ◽  
pp. 21-32 ◽  
Author(s):  
B. I. MORSHED ◽  
M. SHAMS ◽  
T. MUSSIVAND
Keyword(s):  
Transmembrane Potential ◽  
Electric Circuit ◽  
Behavior Modeling ◽  
Equivalent Model ◽  
Passive Components ◽  
Membrane Pores ◽  
Equivalent Models ◽  
Dynamic Components ◽  
Time Invariant ◽  
Transmembrane Resistance

Electroporation is the formation of reversible pores in cell membranes under a brief pulse of high electric field. Dynamics of pore formation during electroporation suggests that the transmembrane potential would settle approximately at the threshold transmembrane potential and the transmembrane resistance would decrease significantly from the state of relaxation. The current electric circuit equivalent models for electroporation containing time-invariant, static and passive components are unable to capture the pore dynamics. A biophysically-inspired electric circuit equivalent model containing dynamic components for membrane pores has been derived using biological parameters. The model contains a voltage-controlled resistor driven by a two-stage cascaded integrator that is activated through a voltage-gated switch. Simulation results with the derived model showed higher accuracy compared to a commonly used model, where the transmembrane resistance decreased million-fold at the onset of electroporation and the transmembrane potential settled at 99.5% of the critical transmembrane potential, thus enabling improved dynamic behavior modeling ability of the pores in electroporation. The derived model allows fast and reliable analysis of this biophysical phenomenon and potentially aids in optimization of various parameters involved in electroporation.

Electroporation of the heart

EP Europace ◽  
2005 ◽  
Vol 7 (s2) ◽  
pp. S146-S154 ◽  
Author(s):  
Vladimir P. Nikolski ◽  
Igor R. Efimov
Keyword(s):  
Electrical Activity ◽  
Tissue Damage ◽  
Transmembrane Potential ◽  
Heart Tissue ◽  
Cardiac Cells ◽  
Electrical Field ◽  
External Electrical Field ◽  
Life Threatening ◽  
Induced Changes

Abstract Defibrillation shocks are commonly used to terminate life-threatening arrhythmias. According to the excitation theory of defibrillation, such shocks are aimed at depolarizing the membranes of most cardiac cells resulting in resynchronization of electrical activity in the heart. If shock-induced changes in transmembrane potential are large enough, they can cause transient tissue damage due to electroporation. In this review evidence is presented that (a) electroporation of the heart tissue can occur during clinically relevant intensities of the external electrical field, and (b) electroporation can affect the outcome of defibrillation therapy; being both pro- and anti-arrhythmic.

scholarly journals Virtual sources associated with linear and curved strands of cardiac cells

2000 ◽  
Vol 279 (4) ◽  
pp. H1579-H1590 ◽  
Author(s):  
Leslie Tung ◽  
André G. Kléber
Keyword(s):  
High Field ◽  
Transmembrane Potential ◽  
Cardiac Cells ◽  
Uniform Electric Field ◽  
Passive Component ◽  
Field Stimulation ◽  
Passive Behavior ◽  
Action Potential Plateau ◽  
Experimental Approaches ◽  
Potential Plateau

Transmembrane potential ( V m) responses in cardiac strands with different curvature were characterized during uniform electric-field stimulation with the use of modeling and experimental approaches. Linear and U-shaped strands (width 100–150 μm) were stained with voltage-sensitive dye. V m was measured by optical mapping across the width and at sites of beginning curvature. Field pulses were applied transverse to the strands during the action-potential plateau. For linear strands, V mcontained 1) a rapid passive component ( V m ar) nearly linear and symmetric across the width, 2) a slower hyperpolarizing component ( V m as) greater and faster on the anodal side, and 3) at high field strengths a delayed depolarizing component ( V m ad) greater on the anodal side. For U-shaped strands, V m at sites of beginning curvature also contained rapid and slow components ( V m br and V m bs, respectively) that included contributions from the linear strand response and from the fiber curvature. V m ar, V m br, and part of V m bs could be attributed to passive behavior that was modeled, and V m as, V m ad, and part of V m bs could be attributed to active membrane currents. Thus curved strands exhibit field responses separable into components with characteristic amplitude, spatial, and temporal signatures.

Effects of electroporation on optically recorded transmembrane potential responses to high-intensity electrical shocks

2004 ◽  
Vol 286 (1) ◽  
pp. H412-H418 ◽  
Author(s):  
V. P. Nikolski ◽  
A. T. Sambelashvili ◽  
V. I. Krinsky ◽  
I. R. Efimov
Keyword(s):  
High Intensity ◽  
Transmembrane Potential ◽  
Cellular Responses ◽  
Rabbit Heart ◽  
Cardiac Cells ◽  
Resting Potential ◽  
Stimulus Strength ◽  
Iodide Uptake ◽  
Electrical Field ◽  
Electrical Shocks

The outcome of defibrillation shocks is determined by the nonlinear transmembrane potential (Δ Vm) response induced by a strong external electrical field in cardiac cells. We investigated the contribution of electroporation to Δ Vm transients during high-intensity shocks using optical mapping. Rectangular and ramp stimuli (10–20 ms) of different polarities and intensities were applied to the rabbit heart epicardium during the plateau phase of the action potential (AP). Δ Vm were optically recorded under a custom 6-mm-diameter electrode using a voltage-sensitive dye. A gradual increase of cathodal and well as anodal stimulus strength was associated with 1) saturation and subsequent reduction of Δ Vm; 2) postshock diastolic resting potential (RP) elevation; and 3) postshock AP amplitude (APA) reduction. Weak stimuli induced a monotonic Δ Vm response and did not affect the RP level. Strong shocks produced a nonmonotonic Δ Vm response and caused RP elevation and a reduction of postshock APA. The maximum positive and maximum negative Δ Vm were recorded at 170 ± 20 mA/cm2 for cathodal stimuli and at 240 ± 30 mA/cm2 for anodal stimuli, respectively (means ± SE, n = 8, P = 0.003). RP elevation reached 10% of APA at a stimulus strength of 320 ± 40 mA/cm2 for both polarities. Strong ramp stimuli (20 ms, 600 mA/cm2) induced a nonmonotonic Δ Vm response, reaching the same largest positive and negative values as for rectangular shocks. The transition from monotonic to nonmonotonic morphology correlates with RP elevation and APA reduction, which is consistent with cell membrane electroporation. Strong shocks resulted in propidium iodide uptake, suggesting sarcolemma electroporation. In conclusion, electroporation is a likely explanation of the saturation and nonmonotonic nature of cellular responses reported for strong electric stimuli.

scholarly journals Influence of Lithium Ions on the Transmembrane Potential and Cation Content of Cardiac Cells

1964 ◽  
Vol 47 (3) ◽  
pp. 501-530 ◽  
Author(s):  
E. E. Carmeliet
Keyword(s):  
Action Potential ◽  
Transmembrane Potential ◽  
Cardiac Cells ◽  
Radioactive Isotopes ◽  
Ion Concentration ◽  
Lithium Ions ◽  
Intracellular Microelectrodes ◽  
Na Ions ◽  
K Permeability ◽  
Action Potential Configuration

The effect of lithium ions on cardiac cells was investigated by recording the changes in transmembrane potential and by following the movement of Li, Na, and K across the cell membrane. Isolated preparations of calf Purkinje fibers and cat ventricular muscles were used. Potentials were measured by intracellular microelectrodes; ion transport was estimated by flame photometric analysis and by using the radioactive isotopes of Na and K. It was shown (a) that Li ions can replace Na ions in the mechanism generating the cardiac action potential but that they also cause a marked depolarization and pronounced changes in action potential configuration; (b) that the resting permeability to Li ions is high and that these ions accumulate in the cell interior as if they were not actively pumped outwards. In Li-Tyrode [K]i decreases markedly while the K permeability seems to be increased. In a kinetic study of net K and Na fluxes, the outward movement of each ion was found to be proportional to the second power of its intracellular concentration. The effect on the transmembrane potential is explained in terms of changes in ion movement and intracellular ion concentration.

Confocal imaging of calcium in intact ventricular muscle provides a new view of excitation-contraction coupling

1996 ◽  
Vol 54 ◽  
pp. 738-739
Author(s):  
W.G. Wier
Keyword(s):  
Local Control ◽  
Cardiac Tissue ◽  
Cell Function ◽  
Isolated Heart ◽  
Cardiac Cells ◽  
Confocal Imaging ◽  
Ion Concentration ◽  
Heart Cell ◽  
Free Calcium ◽  
Heart Cells

A fundamentally new understanding of cardiac excitation-contraction (E-C) coupling is being developed from recent experimental work using confocal microscopy of single isolated heart cells. In particular, the transient change in intracellular free calcium ion concentration ([Ca2+]i transient) that activates muscle contraction is now viewed as resulting from the spatial and temporal summation of small (∼ 8 μm3), subcellular, stereotyped ‘local [Ca2+]i-transients' or, as they have been called, ‘calcium sparks'. This new understanding may be called ‘local control of E-C coupling'. The relevance to normal heart cell function of ‘local control, theory and the recent confocal data on spontaneous Ca2+ ‘sparks', and on electrically evoked local [Ca2+]i-transients has been unknown however, because the previous studies were all conducted on slack, internally perfused, single, enzymatically dissociated cardiac cells, at room temperature, usually with Cs+ replacing K+, and often in the presence of Ca2-channel blockers. The present work was undertaken to establish whether or not the concepts derived from these studies are in fact relevant to normal cardiac tissue under physiological conditions, by attempting to record local [Ca2+]i-transients, sparks (and Ca2+ waves) in intact, multi-cellular cardiac tissue.

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