Electrical Pacing of Cardiac Tissue Including Potassium Inward Rectification.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 26057242.
- Also identified by DOI 10.1371/journal.pone.0127837 and PMC identifier 4461281.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
In this study cardiac tissue is stimulated electrically through a small unipolar electrode. Numerical simulations predict that around an electrode are adjacent regions of depolarization and hyperpolarization. Experiments have shown that during pacing of resting cardiac tissue the hyperpolarization is often inhibited. Our goal is to determine if the inward rectifying potassium current (IK1) causes the inhibition of hyperpolarization. Numerical simulations were carried out using the bidomain model with potassium dynamics specified to be inward rectifying. In the simulations, adjacent regions of depolarization and hyperpolarization were observed surrounding the electrode. For cathodal currents the virtual anode produces a hyperpolarization that decreases over time. For long duration pulses the current-voltage curve is non-linear, with very small hyperpolarization compared to depolarization. For short pulses, the hyperpolarization is more prominent. Without the inward potassium rectification, the current voltage curve is linear and the hyperpolarization is evident for both long and short pulses. In conclusion, the inward rectification of the potassium current explains the inhibition of hyperpolarization for long duration stimulus pulses, but not for short duration pulses.
Medical subject headings
- Cardiac Pacing, Artificial
- Potassium Channels, Inwardly Rectifying