Spontaneous Calcium Release in Cardiac Myocytes: Store Overload and Electrical Dynamics
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Date
2015
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Citation of Original Publication
Alexander, Amanda M.; DeNardo, Erin K.; Frazier, Eric III; McCauley, Michael; Rojina, Nicholas; Coulibaly, Zana; Peercy, Bradford E.; and Izu, Leighton T. (2015) "Spontaneous Calcium Release in Cardiac Myocytes: Store Overload and Electrical Dynamics," Spora: A Journal of Biomathematics: Vol. 1: Iss.1, . DOI: https://doi.org/10.30707/SPORA1.1Alexander
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Abstract
Heart disease is the leading cause of mortality in the United States. One cause of heart arrhythmia is calcium (Ca²⁺) mishandling in cardiac muscle cells. We adapt Izu's et al. mathematical reaction-diffusion model of calcium in cardiac muscle cells, or cardiomyocytes, [14], implemented by Gobbert [12], and analyzed in Coulibaly et al. [8] to include calcium being released from the sarcoplasmic reticulum (SR), the effects of buffers in the SR, particularly calsequestrin, and the effects of Ca²⁺ influx due to voltage across the cell membrane. Based on simulations of the model implemented in parallel using MPI, our findings aligned with
known biological models and principles, giving us a thorough understanding of several factors that influence Ca²⁺ dynamics in cardiac myocytes. Speci cally, dynamic calcium store will cap previous calcium blow-up seen in the model. Calcium channels located in spatial opposition of calcium release units produce more predictable intracellular calcium propagation. And we used multi-parametric calcium dynamics tables, which act as a multidimensional bifurcation diagram, to visualize parameter boundaries between different biophysical dynamics.