Liu Qifeng, Chen Hengsheng, Yu Gengsheng, et al. Changes in sodium channel current of ventricular myocytes in young rats with dilated cardiomyopathy[J]. Journal of Chongqing Medical University, 2016,41(9):923-927.
Liu Qifeng, Chen Hengsheng, Yu Gengsheng, et al. Changes in sodium channel current of ventricular myocytes in young rats with dilated cardiomyopathy[J]. Journal of Chongqing Medical University, 2016,41(9):923-927. DOI: 10.13406/j.cnki.cyxb.000928.
Objective:To investigate the changes in sodium current(I
Na
)of ventricular myocytes in young rats with doxorubicin-induced dilated cardiomyopathy. Methods:Forty SD rats of two-week-old were randomized divided into DCM group(n=20)and control group(n=20). Dilated cardiomyopathy was induced by intraperitoneal injection of doxorubicin 1mg/kg twice a week for six weeks;rats in control group received the injection of normal saline in the same dose. Single ventricular myocyte was isolated from rat heart by enzymatic dissociation and patch clamp technique was used to record the changes of I
Na
in the left ventricular myocytes. Results:The I
Na
of DCM group was potential-dependently reduced
the I-V curve was shifted to upward
and the I
Na
current density in ventricular myocytes was significantly lower in DCM rats than in control rats[(47.370±4.118)p A/p F vs.(64.310±3.278)p A/p F
P=0.003].DCM inhibited the steady-state activation. The half activation potential was raised in DCM rats than in control rats[(-48.441±0.966)m V vs.(-55.132 ± 0.945) m V
P =0.000]
. DCM accelerated the inactivation process. The half inactivation potential was lower in DCM group rather than in control group[(-98.490±1.152)m V vs.(-90.700±1.983)m V
P=0.003)]. The recovery process of I
Na
was unchanged(P=0.617). Conclusion:Doxorubicin-induced DCM can significantly inhibit the steady-state activation
accelerate the inactivation
and decrease I
Na
current density. These changes might lead to cardiac conduction block in DCM.