Electrical heterogeneity of transient outward current in thyroxine induced ventricular myocytes of cardiomyopathy rat
10.3969/j.issn.1000-4718.2010.04.005
- VernacularTitle:甲状腺素性心肌病时左右心室瞬时外向钾电流的不均一性研究
- Author:
Weidong ZHANG
;
Musen LIN
;
Jing WANG
;
Feng YU
- Publication Type:Journal Article
- Keywords:
Electrical heterogeneity;
L-thyroxin;
Cardiomyopathy;
Transient outward potassium current;
Patch-clamp techniques
- From:
Chinese Journal of Pathophysiology
2010;26(4):645-649
- CountryChina
- Language:Chinese
-
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.
