In this thesis we have studied the impact of changing buffering levels in cardiac homeostasis. The heart works by pumping blood through the body by beating. This beating motion originates in the cyclical contraction and relaxation of the muscle walls of the ventricles, which is regulated by calcium concentrations in the myocites. However, changes in calcium levels present are driven by a complex set of interactions with a number of proteins called buffers located mostly in the cytosol, which capture calcium and prevent it from being used in contraction. We have studied this point using a computational biology approach. We have performed simulations with the Multi-Scale Cardiac Simulation Framework (MSCSF), developed at the University of Leeds by Michael A. Colman, which we have suitably modified according to our needs. The main goal of this project has been to change the method by which the amount of calcium bound to buffers is calculated from steady-state approximations to differential equations. This allows for more exact solutions, and, most importantly, conserves calcium mass throughout homeostasis. This way, we have been able to analyse in more detail how these buffers affect excitation-contraction coupling.

In this thesis we have studied the impact of changing buffering levels in cardiac homeostasis. The heart works by pumping blood through the body by beating. This beating motion originates in the cyclical contraction and relaxation of the muscle walls of the ventricles, which is regulated by calcium concentrations in the myocites. However, changes in calcium levels present are driven by a complex set of interactions with a number of proteins called buffers located mostly in the cytosol, which capture calcium and prevent it from being used in contraction. We have studied this point using a computational biology approach. We have performed simulations with the Multi-Scale Cardiac Simulation Framework (MSCSF), developed at the University of Leeds by Michael A. Colman, which we have suitably modified according to our needs. The main goal of this project has been to change the method by which the amount of calcium bound to buffers is calculated from steady-state approximations to differential equations. This allows for more exact solutions, and, most importantly, conserves calcium mass throughout homeostasis. This way, we have been able to analyse in more detail how these buffers affect excitation-contraction coupling.

In this thesis we have studied the impact of changing buffering levels in cardiac homeostasis. The heart works by pumping blood through the body by beating. This beating motion originates in the cyclical contraction and relaxation of the muscle walls of the ventricles, which is regulated by calcium concentrations in the myocites. However, changes in calcium levels present are driven by a complex set of interactions with a number of proteins called buffers located mostly in the cytosol, which capture calcium and prevent it from being used in contraction. We have studied this point using a computational biology approach. We have performed simulations with the Multi-Scale Cardiac Simulation Framework (MSCSF), developed at the University of Leeds by Michael A. Colman, which we have suitably modified according to our needs. The main goal of this project has been to change the method by which the amount of calcium bound to buffers is calculated from steady-state approximations to differential equations. This allows for more exact solutions, and, most importantly, conserves calcium mass throughout homeostasis. This way, we have been able to analyse in more detail how these buffers affect excitation-contraction coupling.