Effect of thyroid hormone on canine cardiac Purkinje fiber transmembrane potential

1981 ◽  
Vol 240 (6) ◽  
pp. H934-H940
Author(s):  
J. M. Jaeger ◽  
S. R. Houser ◽  
A. R. Freeman ◽  
J. F. Spann
Keyword(s):  
Thyroid Hormone ◽  
Action Potential ◽  
Action Potential Duration ◽  
Small Body ◽  
Stimulus Frequency ◽  
Body Weight Loss ◽  
Purkinje Fibers ◽  
Rate Dependent ◽  
Cardiac Purkinje Fibers ◽  
Thyroid Glands

The electrophysiological effects of chronic 3,5,3'-triiodo-L-thyronine (T3) administration on cardiac Purkinje fibers were studied using intracellular recording techniques. Adult mongrel dogs receiving T3 injections (1 mg/kg sc) three times daily for 7-12 days demonstrated elevated resting heart rates and serum total T3 content, atrophied thyroid glands, and a small body weight loss when compared with controls. Isolated Purkinje fibers from control and T3-treated animals were superfused with an oxygenated Tyrode solution containing 4 mM K+ at 35 degrees C. Preparations were stimulated externally at 1.0, 2.0, and 3.1 Hz for 2-3 min while measurements of action potentials were made. At 1.0 Hz, action potential duration (APD) of T3-treated Purkinje fibers was significantly (P less than 0.01) greater than controls at both 20% (APD20) and 80% (APD80) of repolarization to the maximum diastolic potential (Emax). The overshoot, plateau height, and Emax were not different. Raising the stimulus frequency to 2.0 and 3.1 Hz produced a slight increase in the overshoot and a rate-dependent shortening of the action potential duration until it resembled controls. APD20 shortened proportionately more than APD80, giving the action potential a triangular appearance. The K+ selectivity of the resting membrane was not affected as evidenced by Nernst plots, which were identical in normal and T3-treated fibers. These results demonstrate that thyroid hormone influences the action potential of isolated cardiac Purkinje fibers.

Frequency- and voltage-dependent effects of disopyramide in canine Purkinje fibers

1989 ◽  
Vol 67 (7) ◽  
pp. 710-721 ◽  
Author(s):  
Matthew A. Flemming ◽  
Betty I. Sasyniuk
Keyword(s):  
Potassium Channels ◽  
Action Potential ◽  
Sodium Channel ◽  
Action Potential Duration ◽  
Refractory Period ◽  
Drug Effect ◽  
Effective Refractory Period ◽  
Slow Inactivation ◽  
Purkinje Fibers ◽  
Rate Dependent

The voltage- and frequency-dependent blocking actions of disopyramide were assessed in canine Purkinje fibers within the framework of concentrations, membrane potentials, and heart rates which have relevance to the therapeutic actions of this drug. [Formula: see text] was used to assess the magnitude of sodium channel block. Disopyramide produced a concentration- and rate-dependent increase in the magnitude and kinetics of [Formula: see text] depression. Effects on activation time (used as an estimate of drug effect on conduction) were exactly analogous to effects on [Formula: see text]. A concentration-dependent increase in tonic block was also observed. Despite significant increases in tonic block at more depolarized potentials, rate-dependent block increased only marginally with membrane potential over the range of potentials in which propagated action potentials occur. Increases in extracellular potassium concentration accentuated drug effect on [Formula: see text] but attenuated drug effect on action potential duration. Recovery from rate-dependent block followed two exponential processes with time constants of 689 ± 535 ms and 15.7 ± 2.7 s. The latter component represents dissociation of drug from its binding site and the former probably represents recovery from slow inactivation. A concentration-dependent increase in the amplitude of the first component suggested that disopyramide may promote slow inactivation. There was less than 5% recovery from block during intervals equivalent to clinical diastole. Thus, depression of beats of all degrees of prematurity was similar to that of basic drive beats. Prolongation of action potential duration by therapeutic concentrations of drug following a long quiescent interval was minimal. However, profound lengthening of action potential duration occurred following washout of drug effect at a time when [Formula: see text] depression had reverted to normal, suggesting that binding of disopyramide to potassium channels may not be readily reversed. Variable effects on action potential duration may thus be attributed to a block of the window current flowing during the action potential being partially or over balanced by block of potassium channels. Purkinje fiber refractoriness was prolonged in a frequency-dependent manner. Disopyramide did not significantly alter the effective refractory period of basic beats but did increase the effective refractory period of sequential tightly coupled extra stimuli. The results can account for the antiarrhythmic actions of disopyramide during a rapid tachycardia and prevention of its initiation by programmed electrical stimulation.Key words: action potential duration, effective refractory period, upstroke velocity, conduction, rate of sodium channel unblocking.

Effect of norepinephrine on Na(+)-K+ pump and Na+ influx in sheep cardiac Purkinje fibers

1990 ◽  
Vol 258 (4) ◽  
pp. C713-C722 ◽  
Author(s):  
S. W. Chae ◽  
D. Y. Wang ◽  
Q. Y. Gong ◽  
C. O. Lee
Keyword(s):  
Steady State ◽  
Membrane Potential ◽  
Action Potential ◽  
Action Potential Duration ◽  
Relative Magnitude ◽  
Resting Membrane Potential ◽  
Pacemaker Current ◽  
Purkinje Fibers ◽  
Cardiac Purkinje Fibers ◽  
High K

Effects of norepinephrine and Ca+ on Na(+)-K+ pump and pacemaker current were investigated by simultaneous measurement of intracellular Na+ activity (aiNa) and membrane potential in driven (1 Hz) and quiescent sheep cardiac Purkinje fibers. Concurrently, twitch force was measured in driven fibers, in which norepinephrine (NE) produced a decrease in aiNa, a prolongation in action potential duration, and a hyperpolarization in diastolic membrane potential, Vdm. In contrast, in quiescent fibers, NE produced an increase in aiNa and a depolarization in resting membrane potential, Vm. The decrease in aiNa, prolongation in action potential duration, and hyperpolarization in Vdm produced by NE were blocked by 5 x 10(-6) M strophanthidin, presumably through inhibition of the Na(+)-K+ pump. The increase in aiNa and membrane depolarization caused by NE were abolished by high [K+]o or Cs+, presumably through inhibition of the pacemaker current, if. These results indicate that in driven fibers NE stimulates predominantly the Na(+)-K+ pump, producing a decrease in aiNa and that in quiescent fibers it increases predominantly if, producing an increase in aiNa. The effect of NE on driven and quiescent fibers differs because of the voltage dependence of if and perhaps the Na(+)-K+ pump. Consequently, the relative magnitude of the two opposing effects of NE on aiNa appears to be dependent on membrane potential. In quiescent fibers, Cs+ monotonically decreased aiNa to a steady-state value, while Cs+ hyperpolarized membrane potential and then slowly depolarized to a steady-state level, producing a transient hyperpolarization. In driven fibers, Cs+ decreased aiNa, shortened action potential duration, and depolarized Vdm. Cs+ decreased aiNa more in quiescent fibers than in driven fibers. The decrease in aiNa and hyperpolarization in membrane potential produced by Cs+ in quiescent fibers were abolished by depolarization induced by high K+ extracellular concentration (25.4 mM) but were not abolished or reduced by 5 x 10(-6) M strophanthidin. These results suggest that the decrease in aiNa and hyperpolarization in membrane potential by Cs+ are caused by blockage of if but not by stimulation of the Na(+)-K+ pump and that if is an important source of Na+ loading into cells.

Cycle length-dependent action potential duration in canine cardiac Purkinje fibers

1984 ◽  
Vol 247 (6) ◽  
pp. H936-H945 ◽  
Author(s):  
V. Elharrar ◽  
H. Atarashi ◽  
B. Surawicz
Keyword(s):  
Steady State ◽  
Action Potential ◽  
Action Potential Duration ◽  
Cycle Length ◽  
Slow Inward Current ◽  
Tetraethylammonium Chloride ◽  
Inward Current ◽  
Purkinje Fibers ◽  
Cardiac Purkinje Fibers ◽  
Kinetics Of

We studied the effects of pharmacologic probes that affect predominantly the Na inward current [tetrodotoxin (TTX), lidocaine], the slow inward current [cobalt, isoproterenol, verapamil], and the potassium currents [tetraethylammonium chloride (TEA), SG-75] on the duration of the action potential (APD) of canine cardiac Purkinje fibers during steady state and restitution. A schema is proposed in which the APD during steady state or restitution is determined by three factors: maximum action potential duration (APDmax), kinetics of restitution, and “memory.” The predicted APDmax was 469 +/- 34 (SE) ms (n = 27) in control. It was prolonged (P less than 0.05) by cobalt, verapamil, and TEA and shortened (P less than 0.05) by TTX, lidocaine, isoproterenol, and SG-75. In control, the kinetics of restitution were described by a sum of two exponentials with time constant T1 = 137 +/- 9 ms and T2 = 1,665 +/- 135 ms (n = 27), respectively. T1 was prolonged (P less than 0.05) by TTX, lidocaine, and verapamil but was not changed by other probes. None of the probes studied altered the T2 of restitution or the memory factor, computed at a cycle length of 500 ms from the predicted APDmax and the plateau of restitution. Low temperature (31 degrees C) prolonged APDmax and T1 and reduced the memory. We conclude that each of the proposed three factors is controlled by different mechanisms and that a TTX-sensitive current appears to contribute to the process of restitution of APD.

Positive inotropic effect of acetylcholine in canine cardiac Purkinje fibers

1985 ◽  
Vol 249 (4) ◽  
pp. H735-H740 ◽  
Author(s):  
R. F. Gilmour ◽  
D. P. Zipes
Keyword(s):  
Action Potential ◽  
Action Potential Duration ◽  
Force Transducer ◽  
Resting Membrane Potential ◽  
Inotropic Effects ◽  
Purkinje Fibers ◽  
Cardiac Purkinje Fibers ◽  
High Concentrations ◽  
Dose Dependent Increase

The purpose of this study was to investigate possible mechanisms to explain the positive inotropic effects of acetylcholine in canine cardiac Purkinje fibers. Action potentials and tension were recorded from Purkinje fibers in vitro using microelectrodes and a force transducer. Acetylcholine (10(-9) to 10(-4) M) produced a dose-dependent increase in tension that was blocked by atropine but not by propranolol, phentolamine, hexamethonium, or verapamil. At 10(-5) and 10(-4) M, acetylcholine increased action potential duration at 50% of repolarization (APD50) but did not affect resting membrane potential, action potential amplitude, Vmax, or action potential duration at 90% of repolarization (APD90). Isoproterenol (10(-7) M) shortened APD50 and APD90 and increased developed tension. Subsequent addition of acetylcholine (10(-5) M) prolonged APD50 and APD90 and decreased tension. Increasing extracellular Ca2+ concentration [( Ca2+]o) from 2.0 to 3.0 mM increased tension and shortened APD50. Addition of acetylcholine (10(-5) M) increased tension further and prolonged APD50. In K+-depolarized fibers high concentrations of acetylcholine (10(-4) M) restored excitability, but lower concentrations (10(-6) M) suppressed slow responses induced by isoproterenol. Thus acetylcholine alone or with elevated [Ca2+]o increased APD50 and tension and facilitated the induction of slow responses, yet in the presence of isoproterenol acetylcholine increased APD50, decreased tension, and suppressed slow responses. These effects were mediated by muscarinic receptors and were independent of catecholamine release.

Activity-dependent changes in the electrical behaviour of sheep cardiac Purkinje fibres

1985 ◽  
Vol 225 (1241) ◽  
pp. 457-479 ◽  
Keyword(s):  
Action Potential ◽  
Spontaneous Activity ◽  
Action Potential Duration ◽  
Time Course ◽  
Stimulus Frequency ◽  
Similar Time ◽  
Purkinje Fibres ◽  
Pacemaker Potential ◽  
Rate Dependent ◽  
Diastolic Potential

Rate-dependent changes in the electrical activity of sheep Purkinje fibres maintained at 37 °C have been investigated. The duration of the action potential is maximal at a frequency of about 60 min -1 . When the rate is increased above 60 min -1 there is a substantial shortening of the action potential; this occurs abruptly in the first beat at the higher rate although subsequently there can be further changes in duration and these can result in a small prolongation, no change, or a small further shortening of the action potential and can take up to 10 min to reach a steady-state. When the rate is reduced from 60 min -1 there is also a shortening of the action potential but it occurs gradually over several hundred seconds. Action potential duration reaches a minimum value at a rate of about 6 min -1 . 70% of preparations studied showed an increase in duration again at rates below 6 min -1 but duration is always constant at frequencies below about 0.1 min -1 . The maximum diastolic potential is more negative and the pacemaker potential is larger at higher rates of stimulation. When the frequency is raised these variables increase over a time course lasting several hundred seconds. At rates below 60 min -1 the slow changes in action potential duration, maximum diastolic potential and pacemaker potential, after a change in the stimulus frequency, all have similar monoexponential time courses (Ƭ ≈ 3 min) and are accompanied by slow changes in tension production over a similar time course. In Purkinje fibres that exhibit spontaneous activity, rapid stimulation results in overdrive excitation: an acceleration of spontaneous activity when stimulation is ceased.

scholarly journals The effects of acidosis and bicarbonate on action potential repolarization in canine cardiac Purkinje fibers.

1979 ◽  
Vol 73 (2) ◽  
pp. 199-218 ◽  
Author(s):  
K W Spitzer ◽  
P M Hogan
Keyword(s):  
Action Potential ◽  
Action Potential Duration ◽  
Co2 Concentration ◽  
Ionic Currents ◽  
Ph Change ◽  
Purkinje Fibers ◽  
Cardiac Purkinje Fibers ◽  
Carbon Dioxide Co2 ◽  
Diastolic Potential ◽  
Action Potential Repolarization

Studies were performed on canine cardiac Purkinje fibers to evaluate the effects of acidosis and bicarbonate (HCO3) on action potential repolarization. Extracellular pH (pHe) was reduced from 7.4 to 6.8 by increasing carbon dioxide (CO2) concentration from 4 to 15% in a HCO3-buffered solution or by NaOH titration in a Hepes-buffered solution. Both types of acidosis produced a slowing of the rate of terminal repolarization (i.e., period of repolarization starting at about -60 mV and ending at the maximum diastolic potential) with an attendant increase in action potential duration of 10--20 ms. This was accompanied by a reduction in the maximum diastolic potential of 2--8 mV. In contrast, if the same pH change was made by keeping CO2 concentration constant and lowering extracellular HCO3 from 23.7 to 6.0 mM, in addition to the slowing of terminal repolarization, the plateau was markedly prolonged resulting in an additional 50- to 80-ms increase in action potential duration. If pHe was held constant at 7.4 and HCO3 reduced from 23.7 mM to 0 (Hepes-buffered solution), the changes in repolarization were nearly identical to those seen in 6.0 mM HCO3 except that terminal repolarization was unchanged. This response was unaltered by doubling the concentration of Hepes. Reducing HCO3 to 12.0 mM produced changes in repolarization of about one-half the magnitude of those in 6.0 mM HCO3. These findings suggest that in Purkinje fibers, HCO3 either acts as a current that slows repolarization or modulates the ionic currents responsible for repolarization.

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