Parametric study of the Noble’s action potential model for cardiac Purkinje fibers

2007 ◽  
Vol 33 (3) ◽  
pp. 1048-1063 ◽  
Author(s):  
P.K.C. Wang ◽  
B.Y. Kogan
Keyword(s):  
Action Potential ◽  
Parametric Study ◽  
Potential Model ◽  
Purkinje Fibers ◽  
Cardiac Purkinje Fibers

A re-examination of late outward plateau currents of cardiac Purkinje fibers

1985 ◽  
Vol 249 (1) ◽  
pp. H108-H121
Author(s):  
J. M. Jaeger ◽  
W. R. Gibbons
Keyword(s):  
Action Potential ◽  
Voltage Clamp ◽  
Critical Role ◽  
Membrane Current ◽  
Purkinje Fiber ◽  
Purkinje Fibers ◽  
Outward Currents ◽  
Cardiac Purkinje Fibers

Two outward currents, IX1 and IX2, are thought to be activated by depolarization of the Purkinje fiber. One of these, IX1, is presently believed to play a critical role in repolarization of the action potential. The IX currents were originally analyzed in voltage-clamp experiments in sheep Purkinje fibers. These experiments were designed to minimize interference by other currents, and it was assumed that changes of the net current were produced entirely by the IX currents. We have tried to repeat the original experiments and the analysis that led to acceptance of the existence and roles of the IX currents, without success. Moreover, tests of how membrane current should behave if the IX current hypothesis is correct did not give satisfactory results. Our data suggest the original conclusions about IX1 and IX2 may need substantial revision.

Slow inward current may produce many results attributed to IX1 in cardiac Purkinje fibers

1985 ◽  
Vol 249 (1) ◽  
pp. H122-H132
Author(s):  
J. M. Jaeger ◽  
W. R. Gibbons
Keyword(s):  
Action Potential ◽  
Outward Current ◽  
Purkinje Fiber ◽  
Slow Inward Current ◽  
Channel Blockers ◽  
Inward Current ◽  
Purkinje Fibers ◽  
Cardiac Purkinje Fibers ◽  
Current Voltage ◽  
Current Voltage Relation

We have tried to answer two fundamental questions concerning the outward current IX1 of cardiac Purkinje fibers. 1) Is it possible that current changes identified as arising from IX1 in voltage-clamp experiments are actually manifestations of changes in the slow inward current (Isi); and 2) is IX1 in fact required to produce the electrical phenomena attributed to it? Isi behavior and the role of IX1 were explored using computer simulation. The Isi model produced current changes during depolarizations and hyperpolarizations from depolarized resting potentials like those attributed to IX1. It also produced a component of "tail currents" that behaved like IX1. If these current changes were analyzed, assuming that an outward current is responsible, the resulting kinetics and current voltage relation would be very similar to the kinetics and current voltage relation reported for IX1. Using the McAllister, Noble, and Tsien formulation of the Purkinje fiber action potential, we found that IX1 is not essential for repolarization of the reconstructed action potential nor is it needed to reproduce interval duration effects and the effects of applied current in that model. Data suggesting that calcium channel blockers reduce IX1 and that catecholamines increase IX1 may be explained as arising from changes in Isi. Thus many manifestations of IX1 can be explained as arising from unanticipated behavior of Isi, and IX1 does not necessarily play a key role in generating Purkinje fiber electrical activity.

scholarly journals Effect of Formaldehyde and Glutaraldehyde on Electrical Properties of Cardiac Purkinje Fibers

1969 ◽  
Vol 53 (5) ◽  
pp. 530-540 ◽  
Author(s):  
H. A. Fozzard ◽  
G. Dominguez
Keyword(s):  
Action Potential ◽  
Negative Charge ◽  
Input Resistance ◽  
Membrane Resistance ◽  
Rapid Loss ◽  
Purkinje Fibers ◽  
Electrophysiological Properties ◽  
Cardiac Purkinje Fibers ◽  
Length Constant ◽  
Upstroke Velocity

The effects of formaldehyde, glutaraldehyde, 1-fluoro-2,4-dinitrobenzene, and 1,5-difluoro-2,4-dinitrobenzene on the electrophysiological properties of cardiac Purkinje fibers were studied. At concentrations of 2.5 mM the aldehydes produced a transient hyperpolarization, lengthening of the plateau of the action potential, and an increase in action potential overshoot and upstroke velocity. If exposure to aldehyde was continued, the fiber failed to repolarize after an action potential and the membrane potential stabilized at about -30 mv. If exposure was terminated before this, recovery was usually complete. At the time the fibers were hyperpolarized the input resistance was increased without much change in length constant, leading to an increase in both calculated membrane resistance and calculated core resistance. Although it was anticipated that an effect of the aldehydes on the membrane was to increase fixed negative charge, it was difficult to explain all the electrophysiological changes on this basis. The major effects of the fluorobenzene compounds were not the same; they produced a shortening of the action potential and a rapid loss of excitability.

Detection of takeoff potential from intracellular recordings

1982 ◽  
Vol 242 (6) ◽  
pp. H1115-H1117
Author(s):  
R. McGillivray ◽  
R. W. Wald
Keyword(s):  
Electrical Stimulation ◽  
Membrane Potential ◽  
Action Potential ◽  
Cardiac Action Potential ◽  
Intracellular Recordings ◽  
Purkinje Fibers ◽  
Cardiac Action ◽  
Cardiac Purkinje Fibers ◽  
Cardioactive Drugs

The measurement of takeoff potential from intracellular recordings of the cardiac action potential may be useful in the study of the cardiac action potential may be useful in the study of spontaneous automaticity and of the effects of cardioactive drugs on active propagation. We describe a circuit capable of detecting and storing the membrane potential at a point where the slope of the membrane potential exceeds a preset value. The capability of this circuit to track the takeoff potential was tested using intracellular recordings from cardiac Purkinje fibers during spontaneous automaticity as well as during electrical stimulation.

Fetal canine cardiac Purkinje fibers: electrophysiology and ultrastructure

1984 ◽  
Vol 246 (2) ◽  
pp. H250-H260
Author(s):  
P. Danilo ◽  
R. F. Reder ◽  
O. Binah ◽  
M. J. Legato
Keyword(s):  
Action Potential ◽  
Fetal Development ◽  
Late Gestation ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Purkinje Fibers ◽  
Ultrastructural Studies ◽  
Surface Areas ◽  
Cardiac Purkinje Fibers ◽  
External Potassium

We studied the ontogenesis of the transmembrane action potential and the ultrastructure of fetal canine Purkinje fibers. Fetal hearts were obtained from fetuses just after implantation to end gestation. Using standard microelectrode recording techniques, we found that action potential characteristics varied linearly over this period of development. Maximum diastolic potential (MDP) ranged from -65 to -85 mV; action potential amplitude (AMP) varied from 100 to 120 mV; maximum upstroke velocity (Vmax) increased from 200 to 550 V/s. Action potential duration measured to 50% repolarization (APD50) increased from 15 to 156 ms while duration measured at full repolarization (APD100) similarly increased from 75 to 236 ms. The relationship between external potassium concentration and membrane potential was equivalent across all stages of fetal development. Tetrodotoxin (TTX, 7.7 X 10(-7) to 1.6 X 10(-5) M) caused concentration-dependent decreases in AMP, Vmax, and APD50. Verapamil (1 X 10(-7) to 1 X 10(-5) M) decreased Vmax and APD50 in a concentration-dependent manner. The effects of both TTX and verapamil were statistically equivalent across all stages of fetal development. Ultrastructural studies of fetal Purkinje fibers showed that myocytes at the earliest stages of development (Purkinje fibers were not visually distinct at this time) were arranged as a tightly packed mosaic with a rounded shape, with a large amount of glycogen, small sparse mitochondria, and relatively large nuclei. Mitotic cells were observed frequently. Purkinje fibers when first identified grossly had fewer myofilaments than working myocardial cells and sarcomeres without M lines. By late gestation, intercalated disks appeared with an increase in surface areas; desmosomes occurred more frequently. Myofilaments are organized around Z bands into rudimentary sarcomeres that still lack M lines. These data indicate that, although the fetal canine Purkinje fiber undergoes marked developmental changes in ultrastructure, cellular electrophysiological changes are more subtle. The action potential has a qualitative appearance similar to those of the neonatal or adult fiber. At no time during fetal development could we find slow-response action potentials.

Effects of Hypothermia, Potassium, and Verapamil on the Action Potential Characteristics of Canine Cardiac Purkinje Fibers 

1995 ◽  
Vol 82 (3) ◽  
pp. 713-722 ◽  
Author(s):  
Juraj Sprung ◽  
Adam Laszlo ◽  
Lawrence Turner ◽  
John Kampine ◽  
Zeljko Bosnjak
Keyword(s):  
Action Potential ◽  
Antiarrhythmic Effect ◽  
Channel Blockade ◽  
Purkinje Fibers ◽  
Cardiac Action ◽  
Cardiac Purkinje Fibers ◽  
Phase 0 ◽  
Potential Maximum ◽  
Diastolic Potential ◽  
External K

Background Hypothermia may induce hypokalemia and increase intracellular Ca2+ by affecting serum K+ and Ca2+ fluxes across the cell membrane. These ionic alterations may significantly change the electrophysiologic characteristics of the cardiac action potential and may induce cardiac arrhythmias. The current study was undertaken to determine whether electrophysiologic changes in Purkinje fibers induced by hypothermia could be reversed by manipulating the extracellular K+ and transmembrane Ca2+ fluxes by Ca2+ channel blockade with verapamil. Methods A conventional microelectrode method was used to determine the effects of hypothermia (32 +/- 0.5 degrees C and 28 +/- 0.5 degrees C) and various external K+ concentrations ([K+]o) (2.3, 3.8, and 6.8 mM) on maximum diastolic potential, maximum rate of phase 0 depolarization (Vmax), and action potential duration (APD) at 50% (APD50) and at 95% (APD95) repolarization in isolated canine cardiac Purkinje fibers. To evaluate the contribution of the slow inward Ca2+ current to action potential changes in hypothermia, the experiments were repeated in the presence of the Ca(2+)-channel antagonist verapamil (1 microM). Results Variations of [K+]o induced the expected shifts in maximum diastolic potential, and hypothermia (28 degrees C) induced moderate depolarization, but only when [K+]o was > or = 3.9 mM (P < 0.05). Hypothermia decreased Vmax at all [K+]o studied (P < 0.05). Regardless of the temperature, Vmax was not affected by verapamil when [K+]o was < or = 3.9 mM, but at 6.8 mM [K+]o in hypothermia Vmax was significantly lower in the presence of verapamil. Hypothermia increased both the APD50 and the APD95. The effects of verapamil on APD were temperature and [K+]o dependent; between 37 degrees C and 28 degrees C with 2.3 mM [K+]o in the superfusate, verapamil did not affect APD. At 28 degrees C in the presence of verapamil, the APD50 and APD95 decreased only if the [K+]o was > or = 3.9 mM. Conclusions Verapamil and K+ supplementation in hypothermia may exert an antiarrhythmic effect, primarily by reducing the dispersion fo prolonged APD.

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