A newly developed mathematical model successfully reproduced steady-state force-calcium relationships, contraction force time courses, and frequency dependence in mouse ventricular myocytes.
The developed mathematical model accurately simulates mouse ventricular myocyte contraction, highlighting the importance of incorporating variable sarcomere length to reproduce experimental force and shortening dynamics.
Mathematical models of cardiac function at the cellular level include three major components, such as electrical activity, Ca(2+) dynamics, and cellular shortening. We developed a model for mouse ventricular myocyte contraction which is based on our previously published comprehensive models of action potential and Ca(2+) handling mechanisms. The model was verified with extensive experimental data on mouse myocyte contraction at room temperature. In the model, we implemented variable sarcomere length and indirect modulation of the tropomyosin transition rates by Ca(2+) and troponin. The resulting model described well steady-state force-calcium relationships, dependence of the contraction force on the sarcomere length, time course of the contraction force and myocyte shortening, frequency dependence of the contraction force and cellular contraction, and experimentally measured derivatives of the myocyte length variation. We emphasized the importance of the inclusion of variable sarcomere length into a model for ventricular myocyte contraction. Differences in contraction force and cell shortening for epicardial and endocardial ventricular myocytes were investigated. Model applicability for the experimental studies and model limitations were discussed.
Mullins et al. (Thu,) conducted a other in Mouse ventricular myocyte contraction. Mathematical model of mouse ventricular myocyte contraction vs. Experimental data was evaluated on Model accuracy in reproducing experimental data on myocyte contraction. A newly developed mathematical model successfully reproduced steady-state force-calcium relationships, contraction force time courses, and frequency dependence in mouse ventricular myocytes.