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Calcium Oscillations and Ectopic Beats in Virtual Ventricular Myocytes and Tissues: Bifurcations, Autorhythmicity and Propagation

  • Alan P. Benson
  • Arun V. Holden
Part of the Lecture Notes in Computer Science book series (LNCS, volume 3504)

Abstract

One mechanism for the onset of arrhythmias is abnormal impulse initiation such as ventricular ectopic beats. These may be caused by abnormal calcium (Ca2 + ) cycling. The Luo-Rudy model was used to simulate the dynamics of intracellular Ca2 +  ([Ca2 + ]i) handling and the initiation of ectopic beats in virtual ventricular myocytes and tissues. [Ca2 + ]i in the reduced Ca2 +  handling equations settles to a steady state at low levels of intracellular sodium ([Na + ]i), but oscillates when [Na + ]i is increased. These oscillations emerge through a homoclinic bifurcation. In the whole cell, Ca2 +  overload, brought about by inhibition of the sodium-potassium pump and elevated [Na + ]i, can cause autorhythmic depolarisations. These oscillations interact with membrane currents to cause action potentials that propagate through one dimensional virtual tissue strands and two dimensional anisotropic virtual tissue sheets.

Keywords

Sarcoplasmic Reticulum Ectopic Beat Calcium Oscillation Homoclinic Bifurcation Cardiac Action Potential 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer-Verlag Berlin Heidelberg 2005

Authors and Affiliations

  • Alan P. Benson
    • 1
  • Arun V. Holden
    • 1
  1. 1.Computational Biology Laboratory, School of Biomedical SciencesUniversity of LeedsLeedsUK

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