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目的 探讨L型钙通道在急性心肌梗死 (AMI)后室性心律失常发生中的作用及其机制。方法 开胸冠脉结扎制备兔AMI模型 ,于 1周和 2个月处死动物分离心室肌细胞 ,以膜片钳技术记录梗死及周边区心外膜细胞L -型钙通道电流 (ICa -L)的变化。结果 AMI兔梗死周边区心外膜细胞L型钙电流受到抑制 ,电流密度 -电压关系 (I -V)曲线上移 ,其峰值电流密度在正常对照组、AMI后 1周和 2个月分别为 - ( 5 5 8± 1 5 3) pA /pF(n =10 )、- ( 3 5 2± 0 93) pA/ pF (n =6 ,与对照组比较P <0 0 5 )和 - ( 4 84± 1 4 8)pA/ pF(n =11,与对照组比较P <0 0 5 ) ,但I -V曲线的形态轨迹不变。其失活曲线左移 ,失活速度加快 ,半数最大失活电位 3组分别为 -( 13 1± 4 2 )mV、- ( 2 5 9± 7 0 )mV和 - ( 2 1 3± 5 6 )mV ,P <0 0 5。结论 AMI后梗死周边带心外膜细胞L型钙通道受抑制 ,可能为AMI后室性心律失常发生的机制之一 ;AMI后 2个月钙通道的异常程度减轻 ,有恢复正常的趋势
Objective To investigate the role and mechanism of L-type calcium channels in the development of ventricular arrhythmias after acute myocardial infarction (AMI). Methods Rabbit AMI model was established by thoracotomy for coronary artery occlusion. Ventricular myocytes were isolated from animals at 1 week and 2 months. L - type calcium channel current (ICa - L) was measured by patch - clamp technique in the infarct and peripheral epicardial cells. The change. Results The L type calcium currents of epicardial cells in AMI rabbit peripheral area were inhibited and the current density-voltage relationship (I-V) curve was shifted upward. The peak current densities of the epicardial cells in AMI rabbits were significantly higher than those in normal control group and 1 week and 2 months after AMI - (5 5 8 ± 1 5 3) pA / pF (n = 10), - (3 5 2 ± 0 93) pA / pF 84 ± 14 8) pA / pF (n = 11, P <0 05 compared with the control group), but the morphological locus of the I -V curve did not change. The inactivation curve shifted to the left and the inactivation rate was accelerated. The half maximal inactivation potential was - (13 1 ± 4 2) mV, - (2 59 ± 70) mV and - (2 1 3 ± 5 6) ) mV, P <0 0 5. Conclusions The inhibition of L-type calcium channel in epicardial cells around AMI after myocardial infarction may be one of the mechanisms of ventricular arrhythmia after AMI. The abnormalities of calcium channel in 2 months after AMI are relieved and returned to normal