Rice, Jafri, Winslow, 2000

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).

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. (Full text and PDF versions of the article are available for Journal Members on the American Journal of Physiology website.) PubMed ID: 10710361

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.

Derived from workspace Rice, Jafri, Winslow, 2000 at changeset 4533913da7a3.
To begin collaborating on this work, please use your git client and issue this command: