Open AccessSpontaneous Calcium Release in Cardiac Myocytes: Store Overload and Electrical Dynamics
Author(s) -
Amanda M. Alexander,
Erin K. DeNardo,
Eric Frazier,
Michael McCauley,
Nicholas Rojina,
Zana Coulibaly,
Bradford E. Peercy,
Leighton T. Izu
Publication year - 2015
Publication title -
spora a journal of biomathematics
Language(s) - English
Resource type - Journals
eISSN - 2473-5493
pISSN - 2473-3067
DOI - 10.30707/spora1.1alexander
Subject(s) - calcium , myocyte , calcium in biology , biophysics , cardiac muscle , endoplasmic reticulum , chemistry , ryanodine receptor 2 , voltage dependent calcium channel , ryanodine receptor , biology , microbiology and biotechnology , endocrinology , biochemistry , organic chemistry
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 mathematical model (Izu, 2006), implemented by Gobbert (Gobbert, 2008), of cardiac muscle cells, or cardiomyocytes, 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. The mathematical model is coded in C, run using parallel computing (MPI) to efficiently generate simulations of the model, and post-processed in Matlab. Based on computer code and simulations, our findings aligned with known biological models and principles, giving us a thorough understanding of several factors that influence Ca2+ dynamics in cardiac myocytes.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom