Research

PACEMAKING AND NEURAL CONTROL

Brief Summary of Publications (for full text, click on titles)

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Silva, J. and Y. Rudy (2003). "Mechanism of pacemaking in I(K1)-downregulated myocytes." Circ Res 92(3): 261-3.

Biological pacemakers were recently created by genetic suppression of inward rectifier potassium current, IK1, in guinea pig ventricular cells. We simulated these cells by adjusting IK1 conductance in the Luo-Rudy model of the guinea pig ventricular myocyte.

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Dexter, F., M. N. Levy, et al. (1989). "Mathematical model of the changes in heart rate elicited by vagal stimulation." Circ Res 65(5): 1330-9.

We developed a mathematical model of the underlying cellular mechanisms responsible for the changes in sinus cycle length (SCL) elicited by vagal stimulation in intact animals. The model incorporated a stimulation-mediated depletion of the releasable pool of acetylcholine (ACh) in the nerve endings, the in vitro reaction kinetics of acetylcholinesterase, and the electrical activity of a pacemaker cell with six membrane ionic currents.

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Dexter, F., G. M. Saidel, et al. (1989). "Mathematical model of dependence of heart rate on tissue concentration of acetylcholine." Am J Physiol 256(2 Pt 2): H520-6.

The change in sinus period elicited by vagal stimulation depends on the rate of acetylcholine (ACh) release from the nerve endings, the rate of ACh degradation in the nodal tissue, and the responsiveness of the sinus node to ACh. We developed a mathematical model to analyze the dynamics of ACh degradation in the neuroeffector junction and the dependence of sinus period on the concentration of ACh.

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Dexter, F., G. M. Saidel, et al. (1989). "Simulation of the diffusion of acetylcholine in the neuroeffector junctions of the sinus node." J Theor Biol 141(4): 505-14.

Traditionally, the diffusion of acetylcholine (ACh) from a neuron to cardiac muscle in a neuroeffector junction has been modeled as radial diffusion from a nerve ending into a spherical homogeneous medium. Various microscopic structures in the heart may or may not influence the spatial distribution of ACh within neuroeffector junctions. To determine the effect of microscopic anatomy on the diffusion of ACh in neuroeffector junctions, we simulated the diffusion of ACh in a two-dimensional inhomogeneous geometry that was based on micrographs of neuroeffector junctions in the sinus node.

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