Multifractal Desynchronization of the Cardiac Excitable Cell Network During Atrial Fibrillation. II. Modeling

In this study, we elaborate on a tentative interpretation of the observed intermittent dynamics during AF as the signature of synaptic plasticity. Typical individual GJC transition times between open and closed states were shown to be much longer than those of membrane polarization but compare well with membrane recovery time (≳ 100ms) (Spray et al., 1984; Neyton and Trautmann, 1986; Wang et al., 1992; Bukauskas and Verselis, 2004; Desplantez et al., 2007). Moreover, slow gating modulations have been evidenced due to cytoplasmic protons (low pH) and free calcium (Spray et al., 1984; Burt and Sray, 1988; Kumar and Gilula, 1996; Harris, 2001; Bukauskas and Verselis, 2004; Perrachia, 2004; Swietach et al., 2013). Thus, a perturbation of the GJC opening and closing due to electric charge may induce some time lag or advance in the activation of the cell, slowing down or boosting the propagation of the AP, even impeding or reversing it (after reexcitation), resulting in a local departure from ohmic conduction law. Here, we propose a mathematical model of cardiac cell excitability which includes their dynamical coupling by GJC kinetics. As (i) gap junctions electrically bind cardiac cells preferentially along their elongated direction (Severs, 1990; Evans and Martin, 2002)), and (ii) in the left atrial lateral wall area, the CS has a thin surrounding muscular structure traversed by myocardial strands (Ho et al., 2012), we simply consider a one-dimensional (1D) spatial model...
Source: Frontiers in Physiology - Category: Physiology Source Type: research