Changes in anisotropic conduction caused by remodeling cell size and the cellular distribution of gap junctions and Na(+) channels.

摘要: Because gene therapy presents a new frontier in the treatment of arrhythmias, it has become important to know how manipulation cellular distribution proteins changes electrical events within individual cells, and whether these affect conduction at larger macroscopic size scale. However, experimental limitations cardiac bundles prevent measurement delays across specific gap junctions, as well intracellular maximum rate rise action potential (V(max)). In view limitations, we used immunohistochemical morphological results basis develop two-dimensional models neonatal mature canine ventricular muscle order obtain insight into electrophysiological effects proteins; eg, major protein connexin43. Morphological showed that when cells enlarged after birth, junctions shifted from sides ends myocytes. At V(max) was not different during longitudinal transverse propagation. growth hypertrophy produced selective increase mean with no significant change V(max). Two-dimensional computational observed cell accounted for results. The unexpectedly scaling (cell size) is (or more so) junction determining properties suggest pathological states are arrhythmogenic, maintenance remodeling sustaining potential.