ventricular myocyte
electrophysiology
cardiac
The total current of the L-type channel current.
The calcium component of the total L-type channel current.
Catherine Lloyd
Catherine
May
Lloyd
The kinetics of the X gate.
The change in calcium concentration in the junctional sarcoplasmic
reticulum.
A Dynamic Model of the Cardiac Ventricular Action Potential I. Simulations of Ionic Currents and Concentration Changes
74
1096
1071
The University of Auckland, Auckland Bioengineering Institute
The maximum potassium component of the channel's current.
The kinetics of for the j gate.
7514509
The maximum calcium component of the total L-type channel current.
Luo
Ching-hsing
Catherine
May
Lloyd
We need to use dV/dt in the calulation of calcium-induced
calcium-release, so we make it accessible here.
Calculation of the channel reversal potential.
Fixed maths: alpha_J_calculation in fast_sodium_current_j_gate, beta_K1_calculation in time_independent_potassium_current_K1_gate, and i_NaK_calculation in sodium_potassium_pump.
James Lawson
2003-07-30
The time-independent potassium repolarisation current.
The gating kinetics for the channel.
The opening rate for the m gate.
Mammalia
The Luo-Rudy II Model of Mammalian Ventricular Cardiac Action
Potentials, 1994
Ventricular Myocyte
The change in intracellular calcium concentration.
The time-independent inactivation gate for the time-dependent
potassium current - the Xi gate.
Yoram
Rudy
The reversal potential for the channel.
Calculation of the current.
Auckland Bioengineering Institute
The University of Auckland
Catherine
May
Lloyd
The University of Auckland
Auckland Bioengineering Institute
Component grouping together the differential equations for the
various ionic concentrations that the model tracks.
c.lloyd@auckland.ac.nz
Luo
Ching-hsing
7514509
Translocation flux from the network to the junctional sarcoplasmic
reticulum.
keyword
The main component for the model, contains all ionic currents and
defines the transmembrane potential.
This is the CellML description of Luo and Rudy's mathematical model of the mammalian cardiac ventricular action potential. It is a significant development on their original 1991 model. While this version of the model qualitatively compares well to the LR II paper for the action potential, the intracellular calcium dynamics have not been included correctly - namely there is no calcium-induced calcium-release (CICR) process in this version of the model. The original version of the model simulates CICR via a mechanism whereby CICR is induced if and only if the calcium accumulated in the cell in the 2 ms following (dV/dt)max exceeds a given threshold. This sort of process is a bit tricky to include in the CellML (or at least in a way that will work with the CellML abilitites of CMISS) so has been left out for now.
The opening rate of the f gate.
Calculation of the fast sodium current.
The sodium component of the channel's current.
Calculation of the channel conductance.
1071
74
1096
A Dynamic Model of the Cardiac Ventricular Action Potential I. Simulations of Ionic Currents and Concentration Changes
Calculation of the current.
Calcium leak flux from the network sarcoplasmic reticulum into the
cytosol.
The University of Auckland, Auckland Bioengineering Institute
Fixed maths.
The fast sodium current is primarily responsible for the upstroke of
the action potential.
Lloyd
Catherine
May
The potassium component of the total L-type channel current.
The steady-state kinetics of the K1 gate.
The release flux from the junctional sarcoplasmic reticulum into the
cytosol.
This is a dummy equation that we simply use to make grabbing the
value in CMISS much easier.
This is the CellML description of Luo and Rudy's mathematical model of the mammalian cardiac ventricular action potential. It is a significant development on their original 1991 model. While this version of the model qualitatively compares well to the LR II paper for the action potential, the intracellular calcium dynamics have not been included correctly - namely there is no calcium-induced calcium-release (CICR) process in this version of the model. The original version of the model simulates CICR via a mechanism whereby CICR is induced if and only if the calcium accumulated in the cell in the 2 ms following (dV/dt)max exceeds a given threshold. This sort of process is a bit tricky to include in the CellML (or at least in a way that will work with the CellML abilitites of CMISS) so has been left out for now.
The calcium-dependent inactivation gate for the L-type calcium
channel - the fCa gate.
Circulation Research
Circulation Research
The closing rate of the d gate.
The closing rate for the K1 gate.
The maximum sodium component of the channel's current.
The kinetics of the f gate.
Calculation of the channel current.
The sodium component of the total L-type channel current.
The opening rate for the X gate.
The channel reversal potential.
2002-03-28T00:00:00+00:00
1994-06-01
The closing rate for the j gate.
The time-dependent activation gate for the time-dependent potassium
current - the X gate.
The kinetics of the h gate.
The voltage-dependent inactivation gate for the fast sodium channel -
the h gate.
The voltage-dependent inactivation gate for the L-type calcium
channel - the f gate.
Calculation of the release channel conductance. This is incorrect as
there is no CICR induced via the accumulation of calcium in the
cytosol in the period following max(dV/dt)
The opening rate of the d gate.
The kinetics of the m gate.
The sodium-calcium exchanger current, exchanges three sodium ions
for one calcium ion.
2002-03-28
The closing rate for the X gate.
The gating variable for the time-independent potassium current - the K1 gate.
The background sodium current.
The change in intracellular potassium concentration.
The voltage-dependent activation gate for the L-type calcium
channel - the d gate.
The voltage-dependent slow inactivation gate for the fast sodium
channel - the j gate.
The closing rate for the m gate.
1994-06-01
c.lloyd@auckland.ac.nz
Calculation of the exchanger current.
The closing rate for the h gate.
The kinetics of the Xi gate.
The reversal potential for the channel.
The time-dependent potassium reploarisation current.
The reversal potential for the channel.
The change in intracellular sodium concentration.
Calculation of the current.
The maximum potassium component of the total L-type channel current.
A calcium pump for removal of calcium from the cytosol to the
extracellular space.
Yoram
Rudy
A non-specific calcium activated channel - assumed impermeable to
calcium ions but permeable to sodium and potassium ions.
Calculation of the current.
The opening rate for the K1 gate.
The opening rate for the h gate.
The uptake flux into the sarcoplasmic reticulum from the cytosol.
The potassium current active at plateau potentials.
Catherine Lloyd
The L-type calcium channel. Primarily a calcium specific channel,
but with small potassium and sodium components, activated at plateau
potentials.
The change in calcium concentration in the network sarcoplasmic
reticulum.
The various calcium fluxes into and from the sarcoplasmic reticulum.
The calcium pump current.
The total current through the channel.
The background calcium current.
This model contains a delay element in its mathematical description of CICR. Discrete delay elements can not yet be represented in CellML (as of CellML version 1.1) as as such, this model is non-functional.
The closing rate of the f gate.
Calculation of the exchanger current.
2003-06-05
The opening rate for the j gate.
The potassium component of the channel's current.
The maximum sodium component of the total L-type channel current.
The voltage-dependent activation gate for the fast sodium channel -
the m gate.
The sodium/potassium exchanger current which extrudes three sodium
ions from the cell in exchange for two potassium ions entering the
cell.
The reversal potential of the channel.
The kinetics of the fCa gate.
Calculation of reversal potential for the fast sodium channel.
The conductance for the channel.
The kinetics of the d gate.
Assign the rate of change of potential for the differential
equation.