Changes in sodium channel current of ventricular myocytes in young rats with dilated cardiomyopathy

Liu Qifeng; Chen Hengsheng; Yu Gengsheng; Ji Xiaojuan; Bai Yonghong; Cao Lina

doi:10.13406/j.cnki.cyxb.000928

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Changes in sodium channel current of ventricular myocytes in young rats with dilated cardiomyopathy

更新时间：2024-01-17

- Changes in sodium channel current of ventricular myocytes in young rats with dilated cardiomyopathy
- Journal of Chongqing Medical University Vol. 41, Issue 9, Pages: 923-927(2016)
- 作者机构：
  
  重庆医科大学附属儿童医院心内科儿科发育疾病研究教育部重点实验室儿童发育重大疾病国家国际科技合作基地儿科学重庆市重点实验室
- 作者简介：
- 基金信息：
- DOI：10.13406/j.cnki.cyxb.000928
  CLC： R725.4
- Published：2016，
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[1]刘奇峰,陈恒胜,余更生,计小娟,白永虹,曹丽娜.低龄扩张型心肌病鼠心室肌细胞钠电流变化的初步研究[J].重庆医科大学学报,2016,41(09):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 41(9):923-927(2016)
[1]刘奇峰,陈恒胜,余更生,计小娟,白永虹,曹丽娜.低龄扩张型心肌病鼠心室肌细胞钠电流变化的初步研究[J].重庆医科大学学报,2016,41(09):923-927. DOI： 10.13406/j.cnki.cyxb.000928.

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 41(9):923-927(2016) DOI： 10.13406/j.cnki.cyxb.000928.

摘要

目的:探究阿霉素诱导的低龄鼠扩张型心肌病（dilated cardiomyopathy

DCM）模型中心室肌细胞钠电流(sodium current

)的变化。方法:将40只健康的两周龄SD大鼠随机平均分为DCM组（n=20）和对照组（n=20）。DCM组予腹腔注射阿霉素1 mg/kg每周2次

连续6周

诱导建立DCM模型

对照组给予等量生理盐水腹腔注射

以酶解法分离得到单个心室肌细胞

通过全细胞膜片钳技术记录I

、电流-电压（I-V）曲线和钠通道激活、失活和复活的变化情况。结果:与对照组比较

DCM组I

呈电压依赖性减小

I-V曲线上移

电流密度明显下降[（47.370±4.118）p A/p F vs.（64.310±3.278）pA/pF

P=0.003];钠通道激活过程减慢

稳态激活曲线右移

半数稳态激活电压明显升高[（-48.441±0.966）m V vs.（-55.132±0.945）m V

P=0.000]

;失活过程加快

稳态失活曲线左移

半数稳态失活电压降低[（-98.490±1.152）m V vs.（-90.700±1.983）m V

P=0.003];稳态复活曲线与对照组相比无统计学差异（P=0.617）。结论:阿霉素诱导的低龄DCM模型鼠心室肌细胞I

电流密度显著减少

钠通道激活过程减慢

失活过程加快

降低了I

DCM中传导阻滞的发生可能与此有关。

Abstract

Objective:To investigate the changes in sodium current(I

)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

in the left ventricular myocytes. Results:The I

of DCM group was potential-dependently reduced

the I-V curve was shifted to upward

and the I

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

was unchanged（P=0.617）. Conclusion:Doxorubicin-induced DCM can significantly inhibit the steady-state activation

accelerate the inactivation

and decrease I

current density. These changes might lead to cardiac conduction block in DCM.

关键词

钠通道扩张型心肌病膜片钳

Keywords

Sodium channelsdilated cardiomyopathypatch clamp

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Department of Cardiovascular Diseases,The First Affiliated Hospital of Chongqing Medical University

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