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中文摘要：
目的探讨快速延迟整流钾电流（IKr／HERG）在缺血性心律失常发生过程中的调控作用及机制。方法新西兰兔12只，随机分为对照组和缺血组，采用酶解法分离单个心室肌细胞，应用全细胞膜片钳技术记录心室肌细胞IKr／HERG变化趋势；应用Western blot技术，检测转染小RNA（miRNA）后人乳腺癌（SKBr3）细胞IKr／HERG通道蛋白表达量的改变。结果IKr／HERG在实验电压＋60mV下，缺血组（2．25±0．31）pA／pF明显低于对照组（3．81±0．64）pA／pF；miRNA转染进入SKBr3细胞后，细胞膜IKr／HERG通道蛋白表达量降低，仅是对照组的10％。结论miRNA调控IKr／HERG通道蛋白的表达，进而抑制IKr／HERG，参与缺血性心律失常的发生与发展。
英文摘要：
Objective To determine the function and regulatory mechanism of rapid delayed rectifier K^＋ current （IKr/HERG） in the ventricular myocytes of ischemic rabbits. Methods 12 New Zealand rabbits were randomly divided into two groups, ischemic group and control group. Enzyme digestion method was used to isolate single ventricular myocytes and whole cell patch clamp technique was used to record delayed rectifier K^＋ currents. Western blot was also used for examining the expression of IKr/HERG in SKBr3 cells after transient transfection. Results Rapid delayed rectifier K^＋ currents at ＋ 60 mV on ventricutar myocytes in ischemia group was （3.81 ± 0.64） pA/pF vs（2.25 ± 0.31 ） pA/pF in control group. Our data also showed that HERG protein expression was reduced to about 10% of control value after transient transfection. Conclusions The densities of IKr/HERG in the cardiomyocytes of ischemic rabbits were weakened, and the regulation of IKr/HERG plays an important role during ischemia.
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