Abstract
As an important neurotransmitter, acetylcholine (Ach) is closely related with dysfunction of sinoatrial node (SAN), but many questions about its effects on electrophysiological behaviors of SAN are still unclear. In this paper based on the dynamic model of rabbit SAN and atrial cells while considering Ach activated inward rectifying K+ current, other Ach-adjusted ionic currents, and heterogeneity of SAN as well, a two-dimensional tissue model was developed. Computer simulation studies found that slowing of the firing rates caused by Ach could reach above 300%. Upstroke velocity of the central cell is over 3 times greater than that of the peripheral cell, thus presenting more sensitivity to Ach and easier property of sinus pause. Additionally, when Ach distributed nonuniformly, the leading pacemaker site would shift to where the maximum concentration gradient of Ach was. Moreover, the reentrant wave produced at atrial tachycardia could invade into the SAN and suppress its spontaneous firing. The greater the Ach concentration, the easier the suppression is.
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