Mathematical modeling of relations between the kinetics of free intracellular calcium and mechanical function of myocardium.
The paper describes a mathematical model of cardiac muscle contraction based on the assumption of two types of co-operativity which control the formation of calcium-troponin complexes and on a simplified scheme of free intracellular calcium kinetics. Calcium transients are shown to be different in isotonic and isometric conditions, being dependent on initial muscle length as well. Numerical experiments and analysis of the model suggest that calcium uptake by the sarcoplasmic reticulum slows down with an increase in the intracellular concentration of free calcium. This suggestion enables the model to explain the disappearance of load-dependent relaxation observed experimentally at cardiac hypertrophy.
Katsnelson
L B
LB
Institute of Physiology, Russian Academy of Sciences, Ekaterinburg, Russia.
Markhasin
V S
VS
D002118:Calcium / Q000378:metabolism*; D003198:Computer Simulation; D006321:Heart / Q000502:physiology*; D006984:Hypertrophy; D007537:Isometric Contraction; D007700:Kinetics; D008955:Models, Cardiovascular; D009126:Muscle Relaxation; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism; D013997:Time Factors; D014336:Troponin / Q000378:metabolism
D014336:Troponin; D002118:Calcium