ABSTRACT
AIM: To study the electrical heterogeneity of transient outward potassium current (I_(to)) in left and right ventricular myocytes of cardiomyopathy rat. METHODS: The rats were peritoneally injected with L-thyroxine 0.5 mg/kg for 10 d to establish the model of ventricular hypertrophy. The right and left ventricular parts of the heart were separated and the ventricular myocytes were prepared by step digestion using enzyme solution. I_(to) was recorded by using whole cell patch clamp technique. The change of the electrical heterogeneity was determined. RESULTS: The electrical heterogeneity of I_(to) existed in the normal myocytes of left and right ventricles. In the myocytes of left and right ventricles isolated from the cardiomyopathy rats, the electrical heterogeneity was enhanced obviously and showed statistical difference. At +40 mV depolarizing test potential, the current density of I_(to) in the myocytes of right ventricle was increased from (9.23±0.84) pA/pF to (11.19±1.73) pA/pF, while the current density of I_(to) in the myocytes of left ventricle was decreased from (6.99±1.14) pA/pF to (4.95 ±1.84) pA/pF and the dispersion was increased. The V_(1/2) of right ventricle steady inactivation was increased significantly [from (-68.85±1.37) mV to (-49.86±0.69) mV]. The time constant τ of de-inactivation changed significantly [τ left=(79.16±7.04) ms, τ right=(53.19±3.72) ms]. CONCLUSION: Enhanced electrical heterogeneity of I_(to) in the left and right ventricular myocytes of cardiomyopathy rat may represent one of the important ionic mechanisms for some arrhythmia caused by myocardial hypertrophy.
ABSTRACT
Aim: To study the effects of berberine( Ber) on the rapidly activating component( Ⅰ_(Kr)), the slowly activating component(Ⅰ_(Ks)) of the delayed rectifier potassium current and the inward rectifier potassium current(Ⅰ_(K1)) in cardiomyopathic guinea pig ventricular myocytes. Methods: After guinea pigs were ip L-thyroxine 0. 5 mg/kg for 10 d, their hearts were cardiomyopathic. Then whole cell patch-clamp recording technique was used to observe the effect of 30 μmol/L Ber on the Ⅰ_(Kr), Ⅰ_(Ks) and Ⅰ_(K1) in cardiomyopathic guinea pig ventricular myocytes. Results: In cardiomyopathic guinea pig ventricular myocytes, Ber 30 μmol/L markedly inhibited Ⅰ_(Kr) and Ⅰ_(Ks) by 22. 8% and 29. 5% at + 10 mV and + 80 mV, respectively. The effect of Ber on Ⅰ_(Ks) was greater than that on Ⅰ_(Kr). Ber 30 μmol/L also inhibited the inward component of Ⅰ_(K1) by 29. 1% at + 120 mV, but the reverse potential of Ⅰ_(K1) was unaffected. Ber( 1-300 μmol/L) was shown to inhibit Ⅰ_(Kr) and Ⅰ_(Ks) in a concentration-dependent manner. Their IC_(50), were 76. 74 μmol/L and 55. 37 μmol/L, respectively. Conclusion: Ber inhibited Ⅰ_(Kr),Ⅰ_(Ks) and Ⅰ_(K1) in cardiomyopathic guinea pig ventricular myocytes, which may be important in understanding the antiarrhythmic effects of this drug.