Effect of Calcium Concentration on the Transmembrane Potentials of Purkinje Fibers

Temte, John V.; Davis, Larry D.

doi:10.1161/01.res.20.1.32

Cited by 81 publications

(38 citation statements)

References 21 publications

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“…The muscle was pinned to a paraffin block in a tissue bath of 10-ml volume. Modified Tyrode's solution (22), equilibrated in a reservoir with a 95% O 2 -5% CO,, flowed continuously through the bath at a rate of 25 ml/min. Temperature in the tissue bath ranged from 36 to 38°C but remained constant during any experiment.…”

Section: Methodsmentioning

confidence: 99%

“…The maximum rate of rise of the upstroke of the action potential was determined by electronic differentiation. A detailed description of all recording apparatus used in this study appears elsewhere (22).…”

Section: Methodsmentioning

confidence: 99%

“…Methods used to make such measurements have been described previously (22). Solutions of epinephrine hydrochloride (Adrenalin, Parke-Davis Laboratories) were prepared by diluting 1 mg with water to a volume of 25 ml.…”

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confidence: 99%

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Effects of Propranolol on the Transmembrane Potentials of Ventricular Muscle and Purkinje Fibers of the Dog

Davis

Temte

1968

Circulation Research

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195

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Papillary muscle-false tendon tissue preparations isolated from dog hearts were perfused with Tyrode's solution containing propranolol in concentrations ranging from 0.1 to 20.0 mg/liter. Transmembrane action potentials of both ventricular muscle fibers and Purkinje fibers were recorded. With sufficient concentration of drug, the velocity of the upstroke and the overshoot of both fiber types decreased. The curve relating upstroke velocity to level of membrane potential for Purkinje fibers was displaced to the right and down. The ability of both ventricular muscle fibers and Purkinje fibers to respond to rapid frequencies of stimulation was decreased. Repolarization of Purkinje fibers was accelerated by propranolol, but repolarization of ventricular muscle fibers was unaffected. Duration of the effective refractory period of Purkinje fibers decreased; that of ventricular muscle fibers was unchanged. Graded responses and decremental impulse conduction in Purkinje fibers were abolished in the presence of propranolol. Low doses of propranolol which caused no change in the transmembrane potential completely blocked the increase in Purkinje diastolic depolarization normally induced by epinephrine. The possible mechanisms by which propranolol might exert its antiarrhythmic actions on ventricular arrhythmias were discussed. ADDITIONAL KEY WORDS cardiac arrhythmias effective refractory period epinephrine diastolic depolarization rapid electrical stimulation• A number of currently available drugs can block catecholamine beta-receptors (1-5). Many of these compounds exert actions against certain experimentally-induced cardiac arrhythmias. Dichloroisoproterenol, pronethalol, and propranolol prevent the ventricular arrhythmias induced by catecholamines (6-11) and prevent or terminate the ventricular arrhythmias induced by cardiac glycosides (8-16). Other drugs that are unrelated chemically to the above group but also block beta-receptors (4, 5) prevent the arrhythmias induced by catecholamines but not those elicited by cardiac glycosides (8, 9,

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Effects of Propranolol on the Transmembrane Potentials of Ventricular Muscle and Purkinje Fibers of the Dog

Davis

Temte

1968

Circulation Research

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195

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“…Somewhat similar relationships between [Ca 2+ ] o and action potential duration were found for atrial muscle fibers (Hoffman and Suckling, 1956;Hoffman and Cranefield, 1960). For Purkinje fibers, in addition to influencing action potential duration, changes in [Ca 2+ ] o had important effects on threshold potential, on the voltage-dependence of activation of the fast inward channel (gNa) (Weidmann, 1955), and on phase 4 depolarization and automaticity (Hoffman and Suckling, 1956;Weid-mann, 1955;Hoffman and Cranefield, 1960;Temte and Davis, 1967). Also, although changes in [Ca 2+ ] o did not influence membrane resistance (Weidmann, 1955), they did alter the relationship between extracellular potassium concentration [K + ] o and resting potential (Hoffman and Cranefield, 1960).…”

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confidence: 99%

Effects of calcium on canine Purkinje fiber action potential duration in the presence of agents affecting potassium permeability.

Siegal¹,

Hoffman²

1980

Circulation Research

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SUMMARY We used intracellular microelectrodes to study the effect of changes in extracellular calcium ion concentration [Ca 2+ ] o on the transmembrane potentials of canine cardiac Purkinje fibers in control Tyrode's solution and in the presence of agents thought to modify membrane permeability to potassium. In Tyrode's solution, decreasing [Ca 2+ ] o from 2.7 to 0.9 mM increased action potential duration measured at -60 mv (APD «,) and at full repolarization (APDioo) but did not significantly modify the normal linear relationship between cycle length and APD between cycle lengths of 500 to 4000 msec. We used 9-aminoacridine (9-AA) to decrease potassium permeability. At concentrations between 0.01 and 1.5 x 10" 5 M, 9-AA caused a concentration-dependent increase in APD-M and APD 1O o and a significant increase in the slope of the line relating APD to cycle length. (Schiitz, 1936;Cranefield and Hoffman, 1958;Surawicz et al., 1959) and that substitution of other divalent cations such as Sr 2+ for Ca 2+ delays repolarization (Brooks et al., 1955;Garb, 1951). After intracellular microelectrodes were introduced to the study of cardiac electrophysiology, it was shown in most studies that a decrease in [Ca 2+ ] o prolonged and an increase in [Ca 2+ ] o shortened the transmembrane action potential of both ventricular muscle fibers (Hoffman and Suckling, 1956) and Purkinje fibers (Hoffman and Suckling, 1956; Weidmann, 1955). Somewhat similar relationships between [Ca 2+ ] o and action potential duration were found for atrial muscle fibers (Hoffman and Suckling, 1956;Hoffman and Cranefield, 1960 field, 1960). Finally, a number of studies have shown for fibers from sheep and calf hearts that an increase in [Ca 2+ ] o shifts the plateau to more positive potentials and a decrease has the opposite effect (Reuter and Scholz, 1976;Beeler and Reuter, 1970).These effects of [Ca 2+ ] o on action potential duration and on the voltage level of the plateau were difficult to explain in terms of the finding for both Purkinje fibers and ventricular muscle that a significant inward current is carried by Ca 2+ through the secondary or slow inward channels (g si ) and that this current is responsible in large part for maintaining the membrane potential at depolarized levels after the initial action potential upstroke. In terms of these findings one would expect an increase in [Ca 2+ ] o to delay repolarization by increasing inward current and a decrease to have the opposite effect because of the change in driving force for Ca 2+ . An increase in action potential duration in the presence of high [Ca 2+ ] o has been seen only at quite low rates of stimulation (Niedergerke and Orkand, 1972); at usual rates of activation the opposite effect is observed. This apparently anomalous effect of Ca 2+ on action potential duration has been explained by assuming that changes in [Ca 2+ ] o result in changes in [Ca 2+ ]i and that the latter influences the conductance of the membrane by guest on

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“…The contribution of the sodium ion was further minimized in our study by the use of sodiumdeficient Tyrode in which the external and internal sodium concentrations were essentially the same, thus the effect of a change in gNa on resting Vm must be minimal. In normal saline Tyrode solution, an increased membrane conductance due to an increase in either gNa or gCa would result in depolarization of the resting membrane rather than in the observed hyperpolarization, and would increase rather than decrease the slope of slow diastolic depolarization (36). It is difficult, therefore, to assign a major role to the sodium, chloride, or calcium ion which in the presence of an increased membrane conductance could account for the effect of lidocaine on slow diastolic depolarization.…”

Section: Introductionmentioning

confidence: 99%

Effect of lidocaine hydrochloride on membrane conductance in mammalian cardiac purkinje fibers

Mf¹,

Jt²

1972

J. Clin. Invest.

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current-voltage relationships in long Purkinje fibers was corrected for cable complications or when experiments were done in short Purkinje fibers. To minimize complications due to membrane rectifier properties, GK was measured using intracellular application of small hyperpolarizing current pulses as Vm was decreased from -90 to -60 mv by increasing the [K]0 from 3 to 15 mM before and after lidocaine. Lidocaine increased the GK over this range of Vm.These results suggest that lidocaine increases membrane potassium conductance within the range of Vm where the pacemaker potential is seen, an action which can account for its ability to suppress automaticity, and, in part, for its ability to prevent reentrant arrhythmias. INTRODUCTIONThe efficacy of lidocaine hydrochloride in the treatment of cardiac ventricular arrhythmias after open heart surgery, myocardial infarction, and digitalis has been established and recently reviewed (1). Electrophysiologic investigations have shown that in cardiac Purkinje fibers, lidocaine: (a) shortens the action potential duration and decreases the effective refractory period, and (b) exerts an antiautomatic effect by decreasing the slope of slow diastolic depolarization without affecting the maximum diastolic transmembrane voltage (2-4). These observations led Bigger and Mandel to postulate that lidocaine may increase potassium conductance in mammalian cardiac Purkinje fibers (3). The present experiments were designed to test this hypothesis in sheep Purkinje fibers using microelectrode techniques. The effects of lidocaine in a concentration equivalent to clinical plasma antiarrhythmic levels on the transmembrane voltage and on current-voltage relationships suggest that lidocaine does increase potassium conductance in Purkinje fibers.

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Effect of Calcium Concentration on the Transmembrane Potentials of Purkinje Fibers

Cited by 81 publications

References 21 publications

Effects of Propranolol on the Transmembrane Potentials of Ventricular Muscle and Purkinje Fibers of the Dog

Effects of Propranolol on the Transmembrane Potentials of Ventricular Muscle and Purkinje Fibers of the Dog

Effects of calcium on canine Purkinje fiber action potential duration in the presence of agents affecting potassium permeability.

Effect of lidocaine hydrochloride on membrane conductance in mammalian cardiac purkinje fibers

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