Interrelationships Between Automaticity and Conduction in Purkinje Fibers

Microelectrode studies of transmembrane potentials of canine Purkinje fibers show that phase-4 depolarization causes voltage-dependent changes in conduction and responsiveness similar to those occurring during repolarization at comparable levels of potential. Abnormalities ranged from simple slowing of conduction to decrement, unidirectional and bidirectional block, and unexcitability. Reentrant excitation also developed. Significant conduction disturbances usually appeared at −75 to −70 mv; decrement and advanced block at −65 to −60 mv, or below. Because the threshold potential of normal Purkinje cells is approximately −70 mv, depolarization to lower levels implies shifts in this variable toward 0. Determinations of threshold potential confirm such shifts. It may be further inferred that significant abnormalities would most likely occur in fibers in which threshold potential is shifted toward 0 or membrane responsiveness impaired. Alterations in conduction due to phase-4 depolarization provide a reasonable explanation for various peculiarities of cardiac rhythm, including occurrence of conduction disturbances and reentrant rhythms at low heart rates, exit and entry block about parasystolic foci, instability of peripheral Purkinje pacemaakers, and supernormal conduction. Circumstances that enhance phase-4 depolarization are common in diseased hearts, indicating that this mechanism may be a significant factor in human arrhythmias.

[1]  D. Singer,et al.  APPRAISAL OF THE EFFECTS OF CATECHOLAMINES ON CARDIAC ELECTRICAL ACTIVITY * , 1967, Annals of the New York Academy of Sciences.

[2]  A. Kistin Atrioventricular Junctional Premature and Escape Beats with Altered QRS and Fusion , 1966, Circulation.

[3]  A. V. Van Dyke,et al.  Electrophysiological Effects of Isoproterenol on Purkinje Fibers of the Heart , 1966, Circulation research.

[4]  J. Dudel,et al.  Stationary S-shaped current voltage relation and hysteresis in heart muscle fibers. Excitatory phenomena in Na+-free bathing solutions† , 1965 .

[5]  M. Vassalle,et al.  CARDIAC PACEMAKER POTENTIALS AT DIFFERENT EXTRA-AND INTRACELLULAR K CONCENTRATIONS. , 1965, The American journal of physiology.

[6]  W. C. Randall,et al.  Alterations in Cardiac Synchrony Induced by the Cardiac Sympathetic Nerves , 1964, Circulation research.

[7]  E. Moore,et al.  Initiation and conduction of impulses in partially depolarized cardiac fibers. , 1963, The American journal of physiology.

[8]  P. M. Zoll,et al.  Prevention of Ventricular Tachycardia and Fibrillation by Intravenous Isoproterenol and Epinephrine , 1963, Circulation.

[9]  R. Langendorf,et al.  The Supernormal Phase of Atrioventricular Conduction: I. Fundamental Mechanisms , 1962, Circulation.

[10]  T. Walsh Ventricular aberration of A-V nodal escape beats. Comments concerning the mechanism of aberration. , 1962, The American journal of cardiology.

[11]  H. Hecht,et al.  Electrophysiological Study of Human Heart Muscle , 1962, Circulation research.

[12]  W. Trautwein Elektrophysiologie der Herzmuskelfaser , 1961 .

[13]  E. Corday,et al.  Vasopressor therapy for cardiac arrhythmias. , 1961, Diseases of the chest.

[14]  C. Brooks,et al.  Physiology of Atrioventricular Transmission , 1961, Circulation.

[15]  J. Wilkinson,et al.  Clinical Electrocardiography Part I, The Arrhythmias , 1961 .

[16]  W. Greenspan,et al.  The use of vasopressors in cardiac arrhythmias, particularly ventricular tachycardia. , 1961, The American journal of cardiology.

[17]  A. Wallace,et al.  Mechanisms influencing conduction in a case of intermittent bundle branch block. , 1961, American heart journal.

[18]  新楽 和夫 J.C.Slater: Quantum Theory of Atomic Structure, Vol.1, Mc Graw-Hill Book Co., New York 1960, 502頁, 16×23cm, $11. , 1961 .

[19]  R. FitzHugh Thresholds and Plateaus in the Hodgkin-Huxley Nerve Equations , 1960, The Journal of general physiology.

[20]  C. Y. Kao,et al.  Graded and decremental response in heart muscle fibers. , 1958, The American journal of physiology.

[21]  L. Katz,et al.  CLINICAL ELECTROCAHDIOGHAPHY. PART I. THE ARRHYTHMIAS , 1958 .

[22]  A. Pick Aberrant Ventricular Conduction of Escaped Beats: Preferential and Accessory Pathways in the A‐V Junction , 1956, Circulation.

[23]  S. Weidmann,et al.  Effects of calcium ions and local anaesthetics on electrical properties of Purkinje fibres , 1955, The Journal of physiology.

[24]  S. Weidmann,et al.  The effect of the cardiac membrane potential on the rapid availability of the sodium‐carrying system , 1955, The Journal of physiology.

[25]  By David,et al.  Extrasystoles and Allied Arralythmias , 1953, The Indian Medical Gazette.

[26]  A. Hodgkin,et al.  A quantitative description of membrane current and its application to conduction and excitation in nerve , 1952, The Journal of physiology.

[27]  A. Hodgkin,et al.  The dual effect of membrane potential on sodium conductance in the giant axon of Loligo , 1952, The Journal of physiology.

[28]  S. Weidmann,et al.  Effect of current flow on the membrane potential of cardiac muscle , 1951, The Journal of physiology.

[29]  S. Weidmann,et al.  Cardiac resting and action potentials recorded with an intracellular electrode , 1951, The Journal of physiology.

[30]  A. Hodgkin,et al.  The effect of sodium ions on the electrical activity of the giant axon of the squid , 1949, The Journal of physiology.

[31]  F. O. Schmitt,et al.  DIRECTIONAL DIFFERENCES IN THE CONDUCTION OF THE IMPULSE THROUGH HEART MUSCLE AND THEIR POSSIBLE RELATION TO EXTRASYSTOLIC AND FIBRILLARY CONTRACTIONS , 1928 .

[32]  D. Singer,et al.  “New” mode of action of antiarrhythmic agents , 1967 .

[33]  J. Dudel,et al.  [Inhibitory and stimulating action of acetylcholine on the heart of warm-blooded animals; spontaneous generator potential]. , 1958, Pflugers Archiv fur die gesamte Physiologie des Menschen und der Tiere.

[34]  E CORABOEUF,et al.  Temperature effects on the electrical activity of Purkinje fibres. , 1954, Helvetica physiologica et pharmacologica acta.