| pubmed-article:10696706 | pubmed:abstractText | A simulation of the SA node is presented, based on a 2D array (15 x 15) model of randomly distributed pacemaker cells, interacting via a phase response curve (PRC). The model involves only the basic properties that play a direct role in the determination of the SA node rhythm: intrinsic cycle length and PRC. The PRC reflects the 'type' of interaction of each pacemaker cell with the outside world (neighbouring cells, external stimulus, etc.). A major outcome of this study is the demonstration that global dynamics and the degree of 'disorder' of the SA node are strongly affected by the cycle length distribution of the model, as well as spatial inhomogeneity in the cell-to-cell 'electrical' coupling (PRC). Those factors also determine the conduction velocity throughout the SA node and may therefore be responsible for anisotropic conduction. For example, lowering the PRC parameters (d and a) by 25% increases the array activation time from 46 to 126 ms. The model also responds appropriately to a perturbation such as a vagal pulse. This pulse produces a shift of the dominant pacemaker to another site in the array and a transient lengthening of the array cycle length, for example from 312 to 355 ms. | lld:pubmed |
