A model analysis of aftereffects of high-intensity DC stimulation on action potential of ventricular muscle

• Published in: IEEE transactions on biomedical engineering Vol. 45; no. 2; pp. 258 - 267
• Main Authors: Sakuma, I., Haraguchi, T., Ohuchi, K., Fukui, Y., Kodama, I., Toyama, J., Shibata, N., Hosoda, S.
• Format: Journal Article
• Language: English
• Published: New York, NY IEEE 01.02.1998; Institute of Electrical and Electronics Engineers
• Subjects: Action Potentials; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Animals; Associate members; Biological and medical sciences; Biomedical engineering; Biomembranes; Calcium; Cells (biology); Computer Simulation; Defibrillation; Diastole - physiology; Dielectric breakdown; Electric Conductivity; Electric potential; Electric shock; Electric Stimulation; Emergency and intensive cardiocirculatory care. Cardiogenic shock. Coronary intensive care; Intensive care medicine; Mammals; Medical sciences; Membrane Potentials; Models, Cardiovascular; Muscles; Papillary Muscles - physiology; Sodium Channels - metabolism; Ventricular Function; After effect; DC Potential; Electrical properties; Electrical stimulus; Reaction mechanism; Electroporation; Action potential; Heart ventricle; Muscle; Circulatory system; Modeling; Defibrillator
• ISSN: 0018-9294; 1558-2531
• DOI: 10.1109/10.661274

The mechanism for aftereffects of high-intensity dc stimulation on ventricular muscle was studied by using Beeler-Reuter's action potential model. A leak conductance (G/sub pore/ maximal value from 40 to 80 /spl mu/S for 1 cm/sup 2/ of membrane), which mimics reversible dielectric breakdown of the cell membrane by the shock, was incorporated into the model. To simulate resealing process, G/sub pore/ was assumed to decrease after the shock exponentially at a time constant (/spl tau//sub pore/) of 5-50 s. The simulation results are qualitatively consistent with the authors' experimental observations in guinea pig papillary muscle (Amer. J. Physiol., vol. 267, p. H248-58, 1994); they include prolonged depolarization, diastolic depolarization or oscillation of membrane potential leading to a single or multiple spontaneous excitation. The phase-independence and shock intensity-dependence can also be reproduced. Analysis of current components has revealed that: (1) a large inward leak current (l/sub leak/) is responsible for the prolonged depolarization (2) time-dependent decay of outward current (I/sub X1/) in combination with I/sub leak/ and slow inward current (I/sub s/) results in diastolic depolarization or oscillation of membrane potential; (3) spontaneous excitation depends on an activation of I/sub s/. These findings support the authors' hypothesis that strong shocks (>15 V/cm) will produce abnormal arrhythmogenic responses in ventricular muscle through a transient rupture of sarcolemmal membrane.