Background: The effect of fibroblast to electroporation in the aged or diseased heart was unclear. This study used a mathematical model to investigate the fibroblast effect to the myocardium under large premature electrical shock. Methods: The latest 2007 Luo-Rudy ventricular dynamic model was used. The electroporation was described as a transmembrane pore, mimics the reversible breakdown of the cell membrane. 50 times constant basic stimulation was applied to the cell model and the pore formation was carried out at the 50th action potential plateau phase. The pore size was set to occupy 0.15% to 0.25% of the total cell membrane during 10 ms shock. The pore was also assumed to decrease exponentially with a 100-1400ms time constant after shock to simulate the resealing process. Two different fibroblast models were used: the passive fibroblast which connected the model parallel and the active fibroblast with similar membrane capacitance and other ionic currents. Results: Early afterdepolarization and trigger activity were significant increased while increasing either the pore size or resealing time constant. After adding the fibroblast model, the early afterdepolarization was more easily to be induced even with smaller pore size and shorter time constant. Conclusion: Fibroblast electrophysiologically influence the effect of electroporation in ventricular cell, explained the poorer defibrillation outcome in aged or diseased heart.
All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine