i_Stim stim_amplitude time time stim_period stim_period stim_start time time stim_period stim_period stim_start stim_duration 0 time V i_K1 i_to i_Kr i_Ks i_CaL i_NaK i_Na i_b_Na i_NaCa i_b_Ca i_p_K i_p_Ca i_Stim E_Na R T F Na_o Na_i E_K R T F K_o K_i E_Ks R T F K_o P_kna Na_o K_i P_kna Na_i E_Ca 0.5 R T F Ca_o Ca_i alpha_K1 0.1 1 0.06 V E_K 200 beta_K1 3 0.0002 V E_K 100 1 0.1 V E_K 10 1 0.5 V E_K xK1_inf alpha_K1 alpha_K1 beta_K1 i_K1 g_K1 xK1_inf K_o 5.4 V E_K i_Kr g_Kr K_o 5.4 Xr1 Xr2 V E_K xr1_inf 1 1 26 V 7 alpha_xr1 450 1 45 V 10 beta_xr1 6 1 V 30 11.5 tau_xr1 1 alpha_xr1 beta_xr1 time Xr1 xr1_inf Xr1 tau_xr1 xr2_inf 1 1 V 88 24 alpha_xr2 3 1 60 V 20 beta_xr2 1.12 1 V 60 20 tau_xr2 1 alpha_xr2 beta_xr2 time Xr2 xr2_inf Xr2 tau_xr2 i_Ks g_Ks Xs 2 V E_Ks xs_inf 1 1 5 V 14 alpha_xs 1100 1 10 V 6 beta_xs 1 1 V 60 20 tau_xs 1 alpha_xs beta_xs time Xs xs_inf Xs tau_xs i_Na g_Na m 3 h j V E_Na m_inf 1 1 56.86 V 9.03 2 alpha_m 1 1 60 V 5 beta_m 0.1 1 V 35 5 0.1 1 V 50 200 tau_m 1 alpha_m beta_m time m m_inf m tau_m h_inf 1 1 V 71.55 7.43 2 alpha_h 0.057 V 80 6.8 V 40 0 beta_h 2.7 0.079 V 310000 0.3485 V V 40 0.77 0.13 1 V 10.66 11.1 tau_h 1 alpha_h beta_h time h h_inf h tau_h j_inf 1 1 V 71.55 7.43 2 alpha_j 25428 0.2444 V 6.948-6 0.04391 V V 37.78 1 1 0.311 V 79.23 V 40 0 beta_j 0.02424 0.01052 V 1 0.1378 V 40.14 V 40 0.6 0.057 V 1 0.1 V 32 tau_j 1 alpha_j beta_j time j j_inf j tau_j i_b_Na g_bna V E_Na i_CaL g_CaL d f fCa 4 V F 2 R T Ca_i 2 V F R T 0.341 Ca_o 2 V F R T 1 d_inf 1 1 5 V 7.5 alpha_d 1.4 1 35 V 13 0.25 beta_d 1.4 1 V 5 5 gamma_d 1 1 50 V 20 tau_d 1 alpha_d beta_d gamma_d time d d_inf d tau_d f_inf 1 1 V 20 7 tau_f 1125 V 27 2 240 80 165 1 25 V 10 time f f_inf f tau_f alpha_fCa 1 1 Ca_i 0.000325 8 beta_fCa 0.1 1 Ca_i 0.0005 0.0001 gama_fCa 0.2 1 Ca_i 0.00075 0.0008 fCa_inf alpha_fCa beta_fCa gama_fCa 0.23 1.46 tau_fCa 2 d_fCa fCa_inf fCa tau_fCa time fCa 0 fCa_inf fCa V 60 d_fCa i_b_Ca g_bca V E_Ca i_to g_to r s V E_K s_inf 1 1 V 20 5 tau_s 85 V 45 2 320 5 1 V 20 5 3 time s s_inf s tau_s r_inf 1 1 20 V 6 tau_r 9.5 V 40 2 1800 0.8 time r r_inf r tau_r i_NaK P_NaK K_o K_o K_mk Na_i Na_i K_mNa 1 0.1245 0.1 V F R T 0.0353 V F R T i_NaCa K_NaCa gamma V F R T Na_i 3 Ca_o gamma 1 V F R T Na_o 3 Ca_i alpha Km_Nai 3 Na_o 3 Km_Ca Ca_o 1 K_sat gamma 1 V F R T i_p_Ca g_pCa Ca_i Ca_i K_pCa i_p_K g_pK V E_K 1 25 V 5.98 i_rel a_rel Ca_SR 2 b_rel 2 Ca_SR 2 c_rel d g i_up Vmax_up 1 K_up 2 Ca_i 2 i_leak V_leak Ca_SR Ca_i g_inf 1 1 Ca_i 0.00035 6 Ca_i 0.00035 1 1 Ca_i 0.00035 16 d_g g_inf g tau_g time g 0 g_inf g V 60 d_g ddt_Ca_i_total i_CaL i_b_Ca i_p_Ca 2 i_NaCa 2 V_c F Cm i_leak i_up i_rel ddt_Ca_sr_total V_c V_sr i_up i_rel i_leak f_JCa_i_free 1 1 Buf_c K_buf_c Ca_i K_buf_c 2 f_JCa_sr_free 1 1 Buf_sr K_buf_sr Ca_SR K_buf_sr 2 time Ca_i ddt_Ca_i_total f_JCa_i_free time Ca_SR ddt_Ca_sr_total f_JCa_sr_free time Na_i i_Na i_b_Na 3 i_NaK 3 i_NaCa Cm V_c F time K_i i_K1 i_to i_Kr i_Ks i_p_K i_Stim 2 i_NaK Cm V_c F
A Model For Human Ventricular Tissue - M-cell variant Penny Noble Oxford University
Model Status This variant of the model was created by Penny Noble of Oxford University, and represents the parameters given for the M-cell variant in Ten Tusscher et al. 2004. A stimulus protocol component has been added to the model to allow simulation of trains of action potentials. This file is known to run in OpenCell and COR to recreate the published results. The units have been checked and they are consistent.
Model Structure ABSTRACT: The experimental and clinical possibilities for studying cardiac arrhythmias in human ventricular myocardium are very limited. Therefore, the use of alternative methods such as computer simulations is of great importance. In this article we introduce a mathematical model of the action potential of human ventricular cells that, while including a high level of electrophysiological detail, is computationally cost-effective enough to be applied in large-scale spatial simulations for the study of reentrant arrhythmias. The model is based on recent experimental data on most of the major ionic currents: the fast sodium, L-type calcium, transient outward, rapid and slow delayed rectifier, and inward rectifier currents. The model includes a basic calcium dynamics, allowing for the realistic modeling of calcium transients, calcium current inactivation, and the contraction staircase. We are able to reproduce human epicardial, endocardial, and M cell action potentials and show that differences can be explained by differences in the transient outward and slow delayed rectifier currents. Our model reproduces the experimentally observed data on action potential duration restitution, which is an important characteristic for reentrant arrhythmias. The conduction velocity restitution of our model is broader than in other models and agrees better with available data. Finally, we model the dynamics of spiral wave rotation in a two-dimensional sheet of human ventricular tissue and show that the spiral wave follows a complex meandering pattern and has a period of 265 ms. We conclude that the proposed model reproduces a variety of electrophysiological behaviors and provides a basis for studies of reentrant arrhythmias in human ventricular tissue. The original paper reference is cited below: A model for human ventricular tissue, K.H.W.J. ten Tusscher, D. Noble, P.J. Noble, and A.V. Panfilov, 2004, American Journal of Physiology , 286, H1573-H1589. PubMed ID: 14656705 cell diagram A schematic diagram of the Ten Tusscher et al. 2004 mathematical model of the human ventricular myocyte.
cardiac ventricular myocyte electrophysiology K Ten Tusscher H D Noble P Noble J A Panfilov V This variant describes the human cardiac M-cell, as described in ten Tusscher et al. 2004 James Lawson 10000 50000 0.1 1E-8 A model for human ventricular tissue 286 4 1573 1589 American Journal of Physiology Heart and Circulatory Physiology 2004-04-01 10000 10000 0.1 10000 100000 0.1 10000 10000 0.01 keyword 10000 100000 0.01 10000 50000 0.1 unknown 14656705