自发性高血压大鼠肥大心室肌细胞膜离子流的研究

Study on Membrane Ionic Current of Hypertrophied Ventricular Myocytes in Spontaneous Hypertension Rat

目的 研究自发性高血压大鼠肥大左心室肌细胞的膜离子流并探讨其意义。方法 选用自发性高血压大鼠 ,以正常血压Wistar大鼠左心室肌细胞作为对照 ,采用膜片钳全细胞记录技术记录膜离子流 ,观察除极电流 (钠流和L型钙流 )及复极电流 (内向整流性钾流、延迟整流性钾流和瞬间外向性钾流 ) ,并比较其差异。结果 自发性高血压大鼠的心脏重量、心脏重量与体重比及平均细胞膜电容均显著增大 ,钠流、L型钙流及延迟整流性钾流密度无改变 ,然而L型钙流慢失活时间常数显著延长。内向整流性钾流的内向电流密度显著降低 ,瞬间外向性钾流密度显著降低但通道的激活和失活动力学无改变。结论 心脏肥大使左心室肌细胞的重要钾流和钙流发生重构引起复极延迟 。

Objective The ionic remodeling of hypertrophied left ventricular myocytes and its significance were studied. Methods Membrane ionic currents were studied in enzymatically dispersed left ventricular myocytes in spontaneously hypertensive rats(SHRs) with the whole-cell configuration of patch-clamp technique, the depolarizing currents(sodium current, I Na + ;L-type calcium current, I Ca 2+ -L ) and repolarizing currents(inward rectifier potassium current, I K + l ;delayed rectifier potassium current, I K + ;transient outward potassium current, I to ) were observed. The results were compared with that in control of normotension rats. Results Heart weight, ratio of heart weight and body weight, and mean cell membrane capacitance in SHRs were significantly increased. Densities of I Ca 2+ -L , I Na + and I K + in SHRs were not changed, but inactivation time of I Ca 2+ -L was prolonged. Inward component density of I K + l in SHRs was significantly reduced, but outward component density was similar to that in Wistar rat. Density of I to in SHRs was significantly reduced without changes in channel activation and inactivation kinetics. Conclusion Cardiac hypertrophy causes remodeling of important K + and Ca 2+ currents in left ventricular myocytes and it results in repolarization delay. These results demonstrate the important potential implications regarding ventricular arrhythmogenesis.