Acetylcholine lengthens action potentials of sheep cardiac Purkinje fibers

1980 ◽  
Vol 238 (2) ◽  
pp. H237-H243
Author(s):  
S. L. Lipsius ◽  
W. R. Gibbons
Keyword(s):  
Muscarinic Receptors ◽  
Action Potential Duration ◽  
Action Potentials ◽  
Purkinje Fibers ◽  
Diastolic Depolarization ◽  
Cardiac Purkinje Fibers ◽  
Rate Of Increase ◽  
Definite Sequence ◽  
Microelectrode Techniques ◽  
Diastolic Potential

The effect of acetylcholine (ACh) on the electrical activity of sheep cardiac Purkinje fibers was studied using standard microelectrode techniques. Most fibers showed a definite sequence of changes when exposed to ACh. Initially, action potential duration (APD) increased markedly. After about 20 s, the maximum diastolic potential (MDP) started to become more negative and, at the same time, the rate of increase in APD slowed. Once the MDP stabilized at a more negative level, the APD usually resumed its rapid increase. ACh also increased the slope of diastolic depolarization and made the plateau voltage more positive. APD was increased by ACh concentrations as low as 10(-7) M, and it increased with concentrations up to 10(-5) M (the highest concentration tested). ACh-induced increases in APD depended on the stimulation frequency; 2-min exposures to 10(-6) M ACh increased APD by 76.8 +/- 14.7% at 6 min-1 and 17.7 +/- 4.2% at 60 min-1. Atropine blocked all the effects of ACh. Hexamethonium did not prevent the ACh effects. It is concluded that ACh acts via muscarinic receptors. The changes in APD and MDP appear to be separate events, and it is difficult to see how the former effect may be explained by known actions of ACh.

scholarly journals The Electrical Activity of Canine Cardiac Purkinje Fibers in Sodium-Free, Calcium-Rich Solutions

1973 ◽  
Vol 61 (6) ◽  
pp. 786-808 ◽  
Author(s):  
Ronald S. Aronson ◽  
Paul F. Cranefield
Keyword(s):  
Action Potentials ◽  
Transmembrane Potential ◽  
Free Calcium ◽  
Active Response ◽  
Similar Action ◽  
Purkinje Fibers ◽  
Inorganic Cation ◽  
Cardiac Purkinje Fibers ◽  
Diastolic Potential ◽  
Upstroke Velocity

Propagated action potentials can be obtained in canine cardiac Purkinje fibers exposed to Na-free solutions containing no inorganic cation other than Ca and K. Essentially similar action potentials are obtained if Na is replaced by tetraethylammonium (TEA), tetramethylammonium (TMA), or choline. In a solution containing 128 mM TEA and 16.2 mM Ca the characteristics of these electrical responses were: maximum diastolic potential, -59 ± 3.3 mV; overshoot, 20 ± 6.8 mV; maximum upstroke velocity, 3.7 ± 2.3 V/s; conduction velocity, 0.1 m/s; and action potential duration, 360 ± 45 ms. The magnitude of the overshoot varied with log Cao with a slope of about 30 mV/10-fold concentration change. The upstroke velocity was an approximately linear function of Cao. The active response was greatly diminished or abolished by Mn and D-600 but was unaffected by tetrodotoxin. These Ca-dependent responses appeared in a region of transmembrane potential (about -50 mV) at which the rapid Na-dependent upstroke is abolished even when Na is present.

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.

Persistence of the electrophysiologic effects of mexiletine in canine Purkinje fibers alters the response to subsequent hypoxia

1987 ◽  
Vol 65 (10) ◽  
pp. 2104-2109
Author(s):  
Neil D. Berman ◽  
Richard I. Ogilvie ◽  
James E. Loukides
Keyword(s):  
Action Potential ◽  
Action Potential Duration ◽  
Free Solution ◽  
Purkinje Fibers ◽  
Subsequent Exposure ◽  
Hydrochloride Solution ◽  
Drug Free ◽  
Microelectrode Techniques ◽  
Upstroke Velocity ◽  
Normal Formula

The persistence of cellular electropharmacologic effects of mexiletine on canine Purkinje fibers was studied utilizing standard microelectrode techniques and two different protocols. In the first, the tissue was exposed to hypoxic perfusion before and 30 min after perfusion with one of the following: mexiletine hydrochloride 6.25 μM solution, mexiletine hydrochloride 12.5 μM solution, or drug-free Tyrode's solution. With the higher concentration of mexiletine, depression of the maximal upstroke velocity [Formula: see text] persisted 30 min after drug washout and subsequent exposure to hypoxia did not result in the anticipated shortening of action potential duration but did prevent the restoration of normal [Formula: see text]. After perfusion with the lower concentration of mexiletine, [Formula: see text] was not depressed and hypoxic action potential duration shortening was not prevented. In the second protocol, Purkinje fibers were perfused with 12.5 μM mexiletine hydrochloride solution and then exposed to hypoxia after 15, 30,45, or 60 min of perfusion with drug-free solution. Depression of maximal upstroke velocity and shortening of action potential duration persisted during washout, returning to control values by 45 min, although mexiletine was not detectable in the tissue bath after 10 min of washout. Hypoxia initiated at 15 or 30 min of washout failed to produce the anticipated shortening of action potential duration. At 45 and 60 min, action potential duration was shortened by hypoxia. We concluded that mexiletine depression of [Formula: see text] and shortening of action potential duration may persist in the absence of drug. Further shortening of action potential duration in response to hypoxia is prevented during this period. The persistence of [Formula: see text] depression is prolonged by hypoxia.

Effect of acetylcholine on automaticity of canine Purkinje fibers

1976 ◽  
Vol 230 (1) ◽  
pp. 116-119 ◽  
Author(s):  
WW Tse ◽  
J Han ◽  
MS Yoon
Keyword(s):  
Inhibitory Effect ◽  
Appreciable Effect ◽  
Purkinje Fibers ◽  
Spontaneous Rate ◽  
Per Se ◽  
Microelectrode Techniques ◽  
Diastolic Potential

The effect of acetylcholine on automaticity of Purkinje fibers was studied in isolated canine false tendon preparations with conventional microelectrode techniques. Of 15 preparations with the control spontaneous rate of 12-60 beats/min, acetylcholine in a concentration of 0.5 mug/ml decreased the spontaneous rate by 20-87% in 13 preparations. This decrease in automaticity was due to a decrease in the slope of phase 4 depolarization and an increase in the maximum diastolic potential. The inhibitory effect of acetylcholine could be reversed by atropine in a concentration of 3 mug/ml in six preparations and prevented by pretreatment with atropine in another six preparations. Atropine per se did not have any appreciable effect on automaticity of Purkinje fibers. The results indicate that acetylcholine significantly suppresses automaticity of canine Purkinje fibers through its muscarinic action.

Dependence of delayed afterdepolarizations on diastolic potentials in ischemic Purkinje fibers

1989 ◽  
Vol 257 (3) ◽  
pp. H770-H777 ◽  
Author(s):  
W. B. Gough ◽  
N. el-Sherif
Keyword(s):  
Myocardial Infarction ◽  
Action Potentials ◽  
Resting Potential ◽  
Triggered Activity ◽  
Activity Maximum ◽  
Purkinje Fibers ◽  
Sustained Activity ◽  
Delayed Afterdepolarizations ◽  
Diastolic Potential

The mechanism of focal rhythms 1 day after myocardial infarction has been ascribed to both abnormal automaticity and triggered activity arising from delayed after-depolarizations (DADs). During the course of superfusion in vitro, diastolic potentials repolarize to more negative resting potentials. The dependence of DADs and triggered activity on diastolic potentials was studied using extrinsic currents. During sustained activity (maximum diastolic potential = -61 +/- 7 mV), hyperpolarizing current decreased the DADs, rendered them subthreshold, and terminated triggered activity. During the quiescence caused by constant hyperpolarizing current, a stimulated train of action potentials produced DADs. Decreasing the current permitted augmented DADs. In quiescent preparations (resting potential = -68 +/- 7 mV), a train of stimulated action potentials was followed by subthreshold DADs. Depolarizing current increased the DAD amplitude. To exclude depolarization-induced automaticity, constant currents were applied without a previous train of stimuli. Neither DADs nor triggered activity were evoked. Therefore, DADs and triggered activity, postinfarction, depend on the diastolic potential. There is a continuity between subthreshold DADs and sustained activity. DADs may reach a magnitude in which extrinsic interventions may not adequately terminate sustained triggered activity.

Excitability and oscillatory afterpotentials in isolated sheep cardiac Purkinje fibers

1987 ◽  
Vol 252 (3) ◽  
pp. H645-H652 ◽  
Author(s):  
R. M. Terek ◽  
C. T. January
Keyword(s):  
Action Potentials ◽  
Control Level ◽  
Time Dependent ◽  
Resting Potential ◽  
Purkinje Fibers ◽  
Conduction Disturbances ◽  
Cardiac Purkinje Fibers ◽  
Cycle Lengths ◽  
Current Threshold ◽  
The Mean

Oscillatory afterpotentials, or late afterdepolarizations, are one mechanism postulated to cause cardiac arrhythmias and possibly conduction disturbances. We studied excitability by determining strength-interval curves in Purkinje fibers under normal conditions and during the presence of oscillatory afterpotentials induced by cardiac glycoside toxicity. During exposure to acetylstrophanthidin (0.10–0.15 mg/l), the mean resting potential depolarized 5.6 mV and oscillatory afterpotentials of 3–17 mV appeared. Current threshold for evoking action potentials was reduced below control level (e.g., increased excitability) throughout electrical diastole. Associated with oscillatory afterpotentials was a marked biphasic variation in current threshold giving strength-interval curves a characteristic biphasic shape. During the rising phase of the oscillatory afterpotentials, excitability reached a maximum, whereas the minimum increase in excitability occurred during the falling phase of oscillatory afterpotentials. This biphasic change in excitability remained correlated with the oscillatory afterpotentials at different cycle lengths. Results show that during acetylstrophanthidin toxicity excitability is increased throughout electrical diastole, and characteristic time-dependent changes in excitability occur during oscillatory afterpotentials. Time-dependent changes in excitability were detected with both intra- and extracellular stimulation techniques.

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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