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目的:研究5-羟色胺(5-HT)对去甲肾上腺素(NE)诱导的大鼠肥厚心肌L-型钙电流(I_(Ca))的影响.方法:大鼠腹腔注射NE建立心肌肥厚模型;酶解分离单个心室肌细胞;全细胞膜片箝记录I_(Ca).结果:(1)腹腔注射NE第15天,大鼠左心室与体重比增加31.8％(2)肥厚心肌细胞I_(Ca)与正常心肌细胞相比,明显增加0mV时分别为4.5pA/pF±0.5pA/pF和3.5pA/pF±0.3pA/pF(P<0.01).(3)5-HT可显著增加肥厚和正常心肌细胞I_(Ca),并使最大激活电流从0mV降低至-10mV;此外,5-HT增加I_(Ca)作用在肥厚心肌细胞更为显著.(4)稳态激活和失活实验发现,5-HT对稳态激活曲线无显著影响,而影响稳态失活曲线,使半失活电压从-39.5mV±1.8mV升高至-27.8mV±1.7mV(P<0.05),而不改变钙通道电压依赖性(斜率因子k无显著变化).结论:5-HT通过改变L-型钙通道稳态失活特征而显著增加I_(Ca),此作用在肥厚心肌细胞更显著,提示在肥厚心肌5-HT更易于诱导心律失常发生.
Objective: To investigate the effects of 5-hydroxytryptamine (5-HT) on norepinephrine (NE) -induced L-type calcium current (I_ (Ca)) in rat hypertrophic myocardium.Methods: Rat model of myocardial hypertrophy was established by intraperitoneal injection of NE ; Whole cell patch clamp recording I_ (Ca) .Results: (1) On the 15th day after intraperitoneal injection of NE, the ratio of left ventricle to body weight increased by 31.8% (2) ) Were significantly higher than that of normal cardiomyocytes (P <0.01) .5pA / pF ± 0.5pA / pF and 3.5pA / pF ± 0.3pA / pF were significantly increased at 0mV. (3) In addition, 5-HT increased I_ (Ca) in hypertrophic cardiomyocytes more significantly. (4) The steady-state activation and inactivation found that , 5-HT had no significant effect on the steady-state activation curve, but affected the steady-state inactivation curve, raising the half-inactivation voltage from -39.5mV ± 1.8mV to -27.8mV ± 1.7mV (P <0.05) Change the calcium channel voltage dependence (slope factor k no significant change) .Conclusion: 5-HT by changing the steady-state inactivation of L-type calcium channel characteristics significantly increased I_ (Ca), the role of hypertrophic cardiomyocytes more significant, suggesting 5-HT is more likely to induce heart in hypertrophic myocardium Disorders occur.