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

摘要

One mechanism for the onset of arrhythmias is abnormal impulse initiation such as ventricular ectopic beats. These may be caused by abnormal calcium (Ca~(2+)) cycling. The Luo-Rudy model was used to simulate the dynamics of intracellular Ca~(2+) ([Ca~(2+)]_i) handling and the initiation of ectopic beats in virtual ventricular myocytes and tissues. [Ca~(2+)]_i in the reduced Ca~(2+) 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, Ca~(2+) 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.