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Simulating cardiac ventricular action potentials in rat and mouse.

Semahat Demir1

  • 1Program Director, Biomedical Engineering & Research to Aid Persons with Disabilities, Division of Bioengineering and Environmental Systems, National Science Foundation, 4201 Wilson Blvd. Suite 565, Arlington, VA 22230, USA; Faculty of Joint Biomedical Engineering Program, University of Memphis & University of Tennessee, 330 Engineering Technology Building, Memphis TN, 38152-3210, USA.

Conference Proceedings : ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual Conference
|February 7, 2007
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Computational models of rat and mouse cardiac cells reveal key ionic current differences. Action potential variations in rats are linked to transient outward potassium current (It), while mouse repolarization is faster due to delayed rectifier potassium current (IKslow).

Area of Science:

  • Computational biology
  • Cardiac electrophysiology
  • Mammalian cardiovascular research

Background:

  • Computational models are essential for understanding cardiac cell function.
  • Previous models established baseline rat ventricular electrophysiology (Pandit et al., 2001).
  • Existing models provide a foundation for investigating disease states and interspecies differences.

Purpose of the Study:

  • To develop and refine computational models of rat and mouse ventricular cells.
  • To investigate the ionic mechanisms underlying action potential differences in rat ventricles.
  • To identify factors contributing to faster repolarization in mouse ventricular cells compared to rats.

Main Methods:

  • Development of a computational model for rat cardiac ventricular cells using electrophysiology data.

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  • Incorporation of membrane property differences to simulate endocardial and epicardial action potentials.
  • Adaptation of the rat model to create a right ventricular cell model for studying diabetic rat mechanisms.
  • Development of a mouse ventricular cell model based on experimental data and the rat model.

    • Main Results:

    • Action potential changes in rat ventricles (normal, diabetic, aged, hypertensive) are primarily driven by differences in the 4-aminopyridine (4AP) sensitive, calcium-independent transient outward potassium current (It).
    • The presence of the 4AP sensitive, slowly inactivating, delayed rectifier potassium current (IKslow) in mouse ventricular cells significantly contributes to their faster repolarization rate compared to rat cells.

    Conclusions:

    • Differences in transient outward potassium current (It) are the main determinant of action potential variability across rat ventricular regions and in various physiological/pathological states.
    • The delayed rectifier potassium current (IKslow) plays a crucial role in the accelerated repolarization observed in mouse ventricular cells relative to rat ventricular cells.