Electrical Communication in Integrated Arterial Networks

The goal of this investigation was to examine the nature of electrical communication in complex arterial networks and to ascertain how charge distributes within these structures in normal and diseased states. Simulations were performed on an existing computational model expanded to form arterial networks ranging from 1–31 vessels. Initial simulations revealed that focal endothelial stimulation generated responses that conducted along an unbranched vessel with little decay. The introduction of a single branch point augmented electrical decay in a manner dependent on the relative diameter and length of the daughter and parent arteries. These predictions were consistent with experimental observations from the mesentery and support the idea that branch points increase the capacitative load of an arterial network. Further expansion of our virtual network to 31 branches revealed that electrical stimuli could indeed ascend into proximal arteries if a sufficient number of distal arteries were simultaneously activated. Further network analysis centered on the changes in gap junctional conductance which occur during sepsis, hypertension and arthrosclerosis highlighted that each disease state uniquely affects electrical communication and consequently the nature of blood flow control. In summary, this investigation and its synergistic use of computational modeling and experimentation is the first to systematic probe how electrical information spreads in a complex arterial network. Funded by AHFMR and HSFC.