Abstract
Cardiac toxicity caused by organophosphonates (OPs) and expressed through acetylcholine (ACh) overload was studied by simulating the divergence of the action potential (AP) from baseline. Three cardiac structures–the sinoatrial (SA) node, the Purkinje fibers, and the ventricles–were studied with regard to their sensitivity to ACh overload and to determine which is most vulnerable to electrical failure. In addition, based on results of simulations with increased extracellular concentrations, a new model for soman-induced cardiac toxicity is proposed. It was shown that hyperkalemia must be considered in strategies for the prophylaxis of soman poisoning.
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