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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,I_(Na))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_(Na)、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_(Na)呈电压依赖性减小,I-V曲线上移,I_(Na)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_(Na)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_(Na),DCM中传导阻滞的发生可能与此有关。
Objective: To investigate the changes of sodium current (I Na) in doxorubicin - induced dilated cardiomyopathy (DCM) model in isolated rat ventricular myocytes. Methods: Forty healthy two-week-old SD rats were randomly divided into DCM group (n = 20) and control group (n = 20). DCM group was given intraperitoneal injection of doxorubicin 1 mg / kg twice a week for 6 weeks, the induction of DCM model was established, the control group was given an equal volume of saline intraperitoneal injection, enzymatic method was isolated single ventricular myocytes, through the whole cell membrane Forceps technique was used to record changes of I_ (Na), current-voltage (IV) curve and sodium channel activation, inactivation and resuscitation. Results: Compared with the control group, the I_ (Na) in DCM group decreased in a voltage dependent manner, the IV curve shifted up and the current density of Na decreased significantly ([47.370 ± 4.118] p A / p F vs. (64.310 ± 3.278 ) pA / pF, P = 0.003]. The activation of sodium channel slowed down and the steady-state activation curve shifted to the right, and half of the steady-state activation voltage was significantly increased V, P = 0.000]. The inactivation process was accelerated, the steady-state inactivation curve shifted to the left, and half of the steady-state inactivation voltages were decreased [(-98.490 ± 1.152) mV vs (-90.700 ± 1.983) mV, P = 0.003 ]; Steady-state resuscitation curve compared with the control group was no significant difference (P = 0.617). CONCLUSION: Adriamycin induced a significant decrease in I - (Na) current density in ventricular myocytes of young DCM rats, slowing down the activation of sodium channels, inactivating process and decreasing the potential of I Na and conduction block in DCM Related to this.