Figure 1.
Effects of IKr blocker enrythromycin on APD and rate-dependence in myocytes from epicardial (Epi), midmyocardial (M), and endocardial (endo) of canine left ventricle (reproduced from Antzelevitch [5]).
Figure 2.
Alterations of ICa,L kinetics.
The black lines are d∞ and f∞ form Eq.3 with β = 7.2 and Δ = 0. The thick green lines in A are the ones from the original LR1 formulation. The red line in each panel is the altered f∞. A. Δ = 15 mV. B. β = 18. C. Vtrunc = −15 mV.
Figure 3.
Effects of window ICa,L and activation speed of IK on APD.
A. APD vs from the original LR1 model and from the one with 10 mV shift in f∞ (Δ = 10 mV). B. Two action potentials for
= 0.116 mS/cm2 in the original LR1 model and the one with 10 mV shift in f∞. C. ICa,L during the two action potentials in B. D-F. Same as A-C but for γ = 4.
= 0.25 mS/cm2 for E and F. Black arrows in A and D indicate that repolarization failure occurs when
is smaller than these values in the case of Δ = 0 mV (open circles). Green arrows indicate the control
(0.282 mS/cm2). The voltage was initially set to −84 mV with other variables close to their steady states. After 10 s (t = 0 in the plots), a single stimulus was given to elicit an action potential. The same stimulation protocol was used for Figures 4 and 5.
Figure 4.
A. APD vs β for different γ. = 0.15 mS/cm2. B-D. Action potentials for β = 7.2, 10.8, and 18 for the γ = 1(B), γ = 2(C), and γ = 4 (D).
Figure 5.
A. APD vs Vtrunc for different γ. = 0.15 mS/cm2. B. Action potentials for different Vtrunc for γ = 2. C. ICa,L vs time for Vtrunc = 20 mV and −15 mV. D. The activation gate x of IK vs. time for the two action potentials in C.
Figure 6.
Quasi-steady state I-V curves.
A. The quasi-steady state whole-cell current (IQ) vs. voltage in the original model with = 0.15 mS/cm2 with x set at different constant values (as marked). B. IQ vs. voltage with x = 0 for the original model (Δ = 0), 10 mV shift in f∞ (Δ = 10 mV), and f∞ slope reduced (β = 18). C. IQ vs. voltage with x = 0 for different Vtrunc. D. Activation time constant (τx) and the steady-state action curve (x∞) of IK vs. voltage from the original LR1 model.
Figure 7.
A. APD vs. DI for the original model with = 0.15 mS/cm2. γ = 1 (control, black line); γ = 4 (magenta); and γ = 4 and Δ = 10 mV (cyan). B and C. Action potentials at different DIs for γ = 4 and Δ = 0 mV (B) and Δ = 10 mV (C). D. APD vs. DI for β = 18 and γ = 4 (black), and for Vtrunc = −25 mV and γ = 4 (magenta). E. Action potentials at different DIs for β = 18 and γ = 4. F. Action potentials at different DIs for Vtrunc = −25 mV and γ = 4. A single S1 was given the same way as in Figures 3, 4, and 5 and an S2 was given at different S1S2 coupling intervals to study APD rate-dependence.
Figure 8.
APD alternans at slow pacing rates.
A. Action potentials for the original model with = 0.25 mS/cm2 and γ = 4 for three PCLs. B. Same as A but for a reduced slope of f∞ (β = 21.6) with
= 0.2 mS/cm2 and γ = 4. C. Same as A but for a truncated f∞ (Vtrunc = −25 mV) with
= 0.18 mS/cm2 and γ = 4.