AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 278: H452-H460, 2000;
0363-6135/00 $5.00
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Vol. 278, Issue 2, H452-H460, February 2000

Electrical interactions between a real ventricular cell and an anisotropic two-dimensional sheet of model cells

Yang-Gan Wang1, Rajiv Kumar1, Mary B. Wagner1, Ronald Wilders2,3, David A. Golod1, William N. Goolsby1, and Ronald W. Joyner1

1 Todd Franklin Cardiac Research Laboratory, Children's Heart Center, Department of Pediatrics, Emory University, Atlanta, Georgia 30322; 2 Department of Medical Physiology and Sports Medicine, Utrecht University, 3584 CG Utrecht; and 3 Academic Medical Center, Department of Physiology, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands

We have extended our "coupling clamp" technique, in which we couple a real cell to a real-time simulation of a model cell, to now incorporate a real cardiac cell as the central element of a two-dimensional sheet of model cells, in which the coupling conductances may be different in the x and y directions and a specific region of lack of coupling conductance may serve as a resistive barrier. We stimulated the real cell in the central location and determined the critical size of the real cell for successful activation of the entire sheet. We found that this critical size was decreased when anisotropy was present compared with the isotropic case and was further decreased when the central site of stimulation was close to the resistive barrier. The heart normally has some degree of anisotropy, and it has been shown that the remodeling that occurs in peri-infarction zones produces a particular loss of lateral connections compared with end-to-end connections among heart cells. We propose that the normal existence of anisotropy and enhancement of the degree of anisotropy both by loss of lateral gap junctions and the development of resistive barriers may play a facilitating role in the development of ectopic foci that may lead to cardiac arrhythmias.




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