© 1997 American Heart Association, Inc.
Articles |
Ionic Mechanisms of Propagation in Cardiac Tissue
Roles of the Sodium and L-type Calcium Currents During Reduced Excitability and Decreased Gap Junction Coupling
From the Cardiac Bioelectricity Research and Training Center, Case Western Reserve University, Cleveland, Ohio.
Correspondence to Yoram Rudy, Director, Cardiac Bioelectricity Research and Training Center, 505 Wickenden Bldg, Case Western Reserve University, Cleveland, OH 44106-7207. E-mail yxr{at}po.cwru.edu
Abstract In cardiac tissue, reduced membrane excitability and reduced gap junction coupling both slow conduction velocity of the action potential. However, the ionic mechanisms of slow conduction for the two conditions are very different. We explored, using a multicellular theoretical fiber, the ionic mechanisms and functional role of the fast sodium current, INa, and the L-type calcium current, ICa(L), during conduction slowing for the two fiber conditions. A safety factor for conduction (SF) was formulated and computed for each condition. Reduced excitability caused a lower SF as conduction velocity decreased. In contrast, reduced gap junction coupling caused a paradoxical increase in SF as conduction velocity decreased. The opposite effect of the two conditions on SF was reflected in the minimum attainable conduction velocity before failure: decreased excitability could reduce velocity to only one third of control (from 54 to 17 cm/s) before failure occurred, whereas decreased coupling could reduce velocity to as low as 0.26 cm/s before block. Under normal conditions and conditions of reduced excitability, ICa(L) had a minimal effect on SF and on conduction. However, ICa(L) played a major role in sustaining conduction when intercellular coupling was reduced. This phenomenon demonstrates that structural, nonmembrane factors can cause a switch of intrinsic membrane processes that support conduction. High intracellular calcium concentration, [Ca]i, lowered propagation safety and caused earlier block when intercellular coupling was reduced. [Ca]i affected conduction via calcium-dependent inactivation of ICa(L). The increase of safety factor during reduced coupling suggests a major involvement of uncoupling in stable slow conduction in infarcted myocardium, making microreentry possible. Reliance on ICa(L) for this type of conduction suggests ICa(L) as a possible target for antiarrhythmic drug therapy.
Key Words: cardiac excitation • gap junction • cardiac ion channels
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P. Kanagaratnam, S. Rothery, P. Patel, N. J. Severs, and N. S. Peters Relative expression of immunolocalized connexins 40 and 43 correlates with human atrial conduction properties J. Am. Coll. Cardiol., January 2, 2002; 39(1): 116 - 123. [Abstract] [Full Text] [PDF]
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Members of the Sicilian Gambit New Approaches to Antiarrhythmic Therapy, Part I: Emerging Therapeutic Applications of the Cell Biology of Cardiac Arrhythmias Circulation, December 4, 2001; 104(23): 2865 - 2873. [Abstract] [Full Text] [PDF]
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 Members of the Sicilian Gambit New approaches to antiarrhythmic therapy; emerging therapeutic applications of the cell biology of cardiac arrhythmias Eur. Heart J., December 1, 2001; 22(23): 2148 - 2163. [Abstract] [PDF]
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Members of the Sicilian Gambit New approaches to antiarrhythmic therapy: emerging therapeutic applications of the cell biology of cardiac arrhythmias Cardiovasc Res, December 1, 2001; 52(3): 345 - 360. [Abstract] [Full Text] [PDF]
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D. E. Gutstein, G. E. Morley, D. Vaidya, F. Liu, F. L. Chen, H. Stuhlmann, and G. I. Fishman Heterogeneous Expression of Gap Junction Channels in the Heart Leads to Conduction Defects and Ventricular Dysfunction Circulation, September 4, 2001; 104(10): 1194 - 1199. [Abstract] [Full Text] [PDF]
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B. C Eloff, D. L Lerner, K. A Yamada, R. B Schuessler, J. E Saffitz, and D. S Rosenbaum High resolution optical mapping reveals conduction slowing in connexin43 deficient mice Cardiovasc Res, September 1, 2001; 51(4): 681 - 690. [Abstract] [Full Text] [PDF]
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Y. Rudy Multiple interactions determine cellular electrical processes in the multicellular tissue Cardiovasc Res, July 1, 2001; 51(1): 1 - 3. [Full Text] [PDF]
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H. V. M. van Rijen, T. A. B. van Veen, M. J. A. van Kempen, F. J. G. Wilms-Schopman, M. Potse, O. Krueger, K. Willecke, T. Opthof, H. J. Jongsma, and J. M. T. de Bakker Impaired Conduction in the Bundle Branches of Mouse Hearts Lacking the Gap Junction Protein Connexin40 Circulation, March 20, 2001; 103(11): 1591 - 1598. [Abstract] [Full Text] [PDF]
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D. J. Huelsing, A. E. Pollard, and K. W. Spitzer Transient outward current modulates discontinuous conduction in rabbit ventricular cell pairs Cardiovasc Res, March 1, 2001; 49(4): 779 - 789. [Abstract] [Full Text] [PDF]
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D. E. Gutstein, G. E. Morley, H. Tamaddon, D. Vaidya, M. D. Schneider, J. Chen, K. R. Chien, H. Stuhlmann, and G. I. Fishman Conduction Slowing and Sudden Arrhythmic Death in Mice With Cardiac-Restricted Inactivation of Connexin43 Circ. Res., February 16, 2001; 88(3): 333 - 339. [Abstract] [Full Text] [PDF]
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E. Dupont, Y.-S. Ko, S. Rothery, S. R. Coppen, M. Baghai, M. Haw, and N. J. Severs The Gap-Junctional Protein Connexin40 Is Elevated in Patients Susceptible to Postoperative Atrial Fibrillation Circulation, February 13, 2001; 103(6): 842 - 849. [Abstract] [Full Text] [PDF]
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M. A. Allessie, P. A. Boyden, A. J. Camm, A. G. Kleber, M. J. Lab, M. J. Legato, M. R. Rosen, P. J. Schwartz, P. M. Spooner, D. R. Van Wagoner, et al. Pathophysiology and Prevention of Atrial Fibrillation Circulation, February 6, 2001; 103(5): 769 - 777. [Full Text] [PDF]
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C. Cabo, H. Schmitt, and A. L. Wit New Mechanism of Antiarrhythmic Drug Action : Increasing L-Type Calcium Current Prevents Reentrant Ventricular Tachycardia in the Infarcted Canine Heart Circulation, November 7, 2000; 102(19): 2417 - 2425. [Abstract] [Full Text] [PDF]
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Y.-G. Wang, M. B. Wagner, R. Kumar, W. N. Goolsby, and R. W. Joyner Fast pacing facilitates discontinuous action potential propagation between rabbit atrial cells Am J Physiol Heart Circ Physiol, November 1, 2000; 279(5): H2095 - H2103. [Abstract] [Full Text] [PDF]
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A. G. Kleber The fibrillating atrial myocardium. What can the detection of wave breaks tell us? Cardiovasc Res, November 1, 2000; 48(2): 181 - 184. [Full Text] [PDF]
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S. P. Thomas, L. Bircher-Lehmann, S. A. Thomas, J. Zhuang, J. E. Saffitz, and A. G. Kleber Synthetic Strands of Neonatal Mouse Cardiac Myocytes : Structural and Electrophysiological Properties Circ. Res., September 15, 2000; 87(6): 467 - 473. [Abstract] [Full Text] [PDF]
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H. J. Jongsma and R. Wilders Gap Junctions in Cardiovascular Disease Circ. Res., June 23, 2000; 86(12): 1193 - 1197. [Abstract] [Full Text] [PDF]
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J. E. Saffitz, K. G. Green, W. J. Kraft, K. B. Schechtman, and K. A. Yamada Effects of diminished expression of connexin43 on gap junction number and size in ventricular myocardium Am J Physiol Heart Circ Physiol, May 1, 2000; 278(5): H1662 - H1670. [Abstract] [Full Text] [PDF]
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M. Uzzaman, H. Honjo, Y. Takagishi, L. Emdad, A. I. Magee, N. J. Severs, and I. Kodama Remodeling of Gap Junctional Coupling in Hypertrophied Right Ventricles of Rats With Monocrotaline-Induced Pulmonary Hypertension Circ. Res., April 28, 2000; 86(8): 871 - 878. [Abstract] [Full Text] [PDF]
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Y. Wang and Y. Rudy Action potential propagation in inhomogeneous cardiac tissue: safety factor considerations and ionic mechanism Am J Physiol Heart Circ Physiol, April 1, 2000; 278(4): H1019 - H1029. [Abstract] [Full Text] [PDF]
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