Modelling Interval-Force Relations in Cardiac Muscle
Catherine
Lloyd
Bioengineering Institute, University of Auckland
Model Status
This is the original unchecked version of the model imported from the previous
CellML model repository, 24-Jan-2006.
Model Structure
Short-term interval-force (I-F) relations describe the dependence of cardiac muscle contraction strength for short interbeat intervals. Two phenomena that characterise these short-term I-F relations are restitution and postextrasystolic potentiation. In their 2000 paper, J. Jeremy Rice, M. Saleet Jafri and Raimond L. Winslow use two modelling approaches to study short-term interval-force relations in cardiac muscle. Their first approach employs a relatively simple (or minimal), discrete-time model of excitation-contraction coupling. This model explains restitution and postextrasystolic potentiation in terms of the total amount of Ca2+ stored in the sarcoplasmic reticulum (SR) and a feature in which Ca2+ stored in the SR slowly becomes available for release into the sarcoplasm (see below).
simple_model
Schematic diagram of a simple, discrete-time model of Ca2+-handling in restitution and postextrasystolic potentiation. InSC and OutSC represent Ca2+ influx and efflux across the sarcolemma, and InSR and OutSR represent sarcoplasmic reticulum Ca2+ release and uptake.
In their second modelling approach, J. Jeremy Rice, M. Saleet Jafri and Raimond L. Winslow develop a more detailed ventricular cell model that is able to simulate action potentials, Ca2+-handling mechanisms, and isometric force generation by the myofilaments. This single comprehensive (or maximal) model combines two previously developed models (see The Jafri-Rice-Winslow Ventricular Model, 1998 and Cooperative Mechanisms in Cardiac Muscle, Rice et al., 1999). The first ventricular cell model describes membrane currents and Ca2+-handling, and the second model of myofilaments provides the force generation of muscle contraction (see below). The ventricular cell model provides the Ca2+ needed to drive the myofilament contraction. This is a feedforward pathway in which Ca2+ binds to troponin and initiates force generation by triggering myofilament contraction. A feedback pathway also links the two models, as the affinity of troponin for Ca2+ is a function of developed force.
Modeling short-term interval-force relations in cardiac muscle, J. Jeremy Rice, M. Saleet Jafri and Raimond L. Winslow, 2000, American Journal of Physiology, 278, H913-H931. PubMed ID: 10710361
detailed_model
Schematic diagram of a detailed, single ventricular cell model which is able to simulate action potentials, Ca2+-handling and isometric force generation by myofilaments.
Simulation results generated from the model support experimental data. They suggest that short-term interval-force relations result mainly from the interplay between ryanodine receptor adaptation and SR Ca2+ loading with additional contributions from membrane currents and myofilament activation.
calcium dynamicscardiac myocyteCardiac Myocyteelectrophysiologymyofilament mechanicscardiackeywordAmerican Journal of Physiology: Heart and Circulatory Physiology
The Rice et al's 2000 detailed model of ventricular cardiac
myocytes
Cardiac MyocyteThis is the CellML description of Rice et al's 2000 detailed model of ventricular cardiac myocytes. It simulates action potentials, Ca2+-handling mechanisms and isometric force generation by the myofilaments.10710361RaimondWinslowLMJafriSaleetCatherine Lloyd2000-03-01Modeling short-term interval-force relations in cardiac muscle278H913H931JohnRiceJeremy