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(Circulation Research. 1998;83:1003-1014.)
© 1998 American Heart Association, Inc.

Original Contributions

Spatial Changes in the Transmembrane Potential During Extracellular Electric Stimulation

Xiaohong Zhou, Stephen B. Knisley, William M. Smith, Dennis Rollins, Andrew E. Pollard, , Raymond E. Ideker

From the Division of Cardiovascular Disease, Department of Medicine (X.Z., W.M.S., D.R., R.E.I.), Department of Biomedical Engineering (S.B.K., W.M.S., A.E.P., R.E.I.), and Department of Physiology (R.E.I.), University of Alabama at Birmingham, Birmingham, Ala.

Correspondence to Xiaohong Zhou, MD, B140 Volker Hall, Box 201, University of Alabama at Birmingham, Birmingham, AL 35294-0019. E-mail xhz{at}crml.uab.edu

Abstract—The purpose of this study was to determine the spatial changes in the transmembrane potential caused by extracellular electric field stimulation. The transmembrane potential was recorded in 10 guinea pig papillary muscles in a tissue bath using a double-barrel microelectrode. After 20 S1 stimuli, a 10-ms square wave S2 shock field with a 30-ms S1–S2 coupling interval was given via patch shock electrodes 1 cm on either side of the tissue during the action potential plateau. Two shock strengths (2.1±0.2 and 6.5±0.6 V/cm) were tested with both shock polarities. The recording site was moved across the tissue along fibers with either 200 µm (macroscopic group [n=5], 12 consecutive recording sites over a 2.2-mm tissue length in each muscle) or 20 µm (microscopic group [n=5], 21 consecutive recording sites over a 0.4-mm tissue length in each muscle) between adjacent recording sites. In the macroscopic group, the portion of the tissue toward the anode was hyperpolarized, whereas the portion toward the cathode was depolarized, with 1 zero-potential crossing from hyperpolarization to depolarization present near the center of the tissue. In the microscopic group, only 1 zero-potential crossing was observed in the center region of the tissue, whereas, away from the center, only hyperpolarization was observed toward the anode and depolarization toward the cathode. Although these results are consistent with predictions from field stimulation of continuous representations of myocardial structure, ie, the bidomain and cable equation models, they are not consistent with the prediction of depolarization-hyperpolarization oscillation from representations based on cellular-level resistive discontinuities associated with gap junctions, ie, the sawtooth model.

Key Words: hyperpolarization • defibrillation • simulation

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