Skip to main content
. 2013 Mar;10(1):39–51. doi: 10.3969/j.issn.1671-5411.2013.01.008

Figure 6. The gating mechanism of IKr in the three groups of rabbit ventricular cardiomyocytes.

Figure 6.

The steady-state activated curve of the three groups were not markedly different (A-C), while steady-state inactivated curves for HMI and HMI + NGF cardiomyocytes were shifted negative, with a V1/2,inact shifted from -21.6 ± 3.2 mV for the Ctrl group to -46.2 ± 7.2 mV in the HMI group, -50.7 ± 6.1 mV in the HMI+NGF group (D-F). The time constant of fast inactivation (IKr) for HMI and HMI + NGF cardiomyocytes was shorter than that of Ctrl cardiomyocytes (G). In contrast, the time constant of recovery from inactivation of IKr for HMI and HMI + NGF cardiomyocytes was longer than that of Ctrl cardiomyocytes at range from -120 mV to -30 mV (H). *P < 0.01 vs. Ctrl cardiomyocytes, #P < 0.01 vs. HMI group. Ctrl: control; HMI: healed myocardial infarction; IKr: rapidly activated component of delayed rectifier potassium current; NGF: nerve growth factor.