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目的为探讨心力衰竭(简称心衰)兔左室短暂外向钾电流(Ito)下调的分子基础。方法采用结扎家兔冠状动脉左前降支的方法制备缺血性心衰模型。应用膜片钳全细胞记录方法记录左室心肌细胞Ito,描记电流-电压(I-V)曲线;应用半定量-聚合酶链式反应(RT-PCR)法检测电压依赖性Kv1.4和Kv4.3钾通道α亚单位mRNA表达,并以图象分析系统对其进行半定量分析。结果心衰组家兔左室心肌细胞Ito密度较对照组显著降低,I-V曲线明显下移;指令电压为+70mV时,心衰组Ito密度(9.73±0.94pA/pF,n=5)显著低于对照组(14.35±1.16pA/pF,n=4)(P<0.01)。Kv1.4和Kv4.3钾通道α亚单位mRNA表达心衰组(分别为0.66±0.05,0.21±0.02,n=5)也较对照组(分别为0.95±0.07,0.531±0.04,n=5)显著降低(P均<0.01)。结论心衰家兔左室Ito电流密度下调可能受转录水平调节。
Objective To investigate the molecular basis of left ventricular outward outward potassium current (Ito) down-regulation in heart failure (HF). Methods The model of ischemic heart failure was made by ligation of left anterior descending coronary artery in rabbits. The patch-clamp whole-cell recording method was used to record Ito of left ventricular myocytes and the current-voltage (IV) curve was recorded. The voltage-dependent Kv1.4 and Kv4.3 were detected by semi-quantitative polymerase chain reaction (RT- Potassium channel α subunit mRNA expression was analyzed semiquantitatively with image analysis system. Results The Ito density of left ventricular myocytes of rabbits with heart failure was significantly lower than that of the control group and the IV curve was significantly decreased. The Ito density of heart failure group (9.73 ± 0.94pA / pF, n = 5) was significantly lower at the command voltage of +70 mV In the control group (14.35 ± 1.16 pA / pF, n = 4) (P <0.01). Kv1.4 and Kv4.3 potassium channel α subunit mRNA expression in HF group (0.66 ± 0.05,0.21 ± 0.02, n = 5, respectively) were also significantly lower than those in the control group (0.95 ± 0.07, 0.531 ± 0.04, n = 5 ) Were significantly lower (all P <0.01). Conclusions The decrease of Ito current density in left ventricle of rabbits with heart failure may be regulated by transcriptional level.