缺血/再灌注对心肌细胞瞬间外向钾电流的影响

Effects of ischemia/reperfusion of transient outward potassium current of rat myocytes

目的探讨在心肌缺血/再灌注后,瞬间外向钾电流(transientoutsidepotassiumcurrent,Ito)的变化及其在室性心律失常发生中的作用。方法以常规方法制备大鼠心肌缺血/再灌注模型,以酶解法分离单个心室肌细胞,采用全细胞膜片钳记录技术观察缺血10min和30min后,再灌注组的心室肌细胞Ito的变化,以正常心肌的Ito为对照组。结果缺血/再灌注组心室肌细胞Ito电流密度$C电压关系曲线下移,+70mV的Ito密度对照组为52.2±12.1pA/pF(n=11cells),缺血10min和30min再灌注组分别为7.2±2.5pA/pF(n=9cells)和6.4±2.7pA/pF(n=10cells),与对照组相比有显著性差异(P<0.01)。其失活曲线右移,半数最大失活电位对照组为-60±14mV(n=9cells),缺血10min和30min再灌注组分别为-58±12mV(n=8cells)和-50±12mV(n=9cells),与对照组比较,缺血30min再灌注组显著减小(P<0.05),而缺血10min再灌注组变化不明显(P>0.05)。缺血10min再灌注组Ito失活后再恢复过程较对照组显著减慢(P<0.05),而缺血30min再灌注组有恢复趋势。结论缺血/再灌注心室肌细胞瞬间外向钾电流受抑制,可能为缺血/再灌注性心律失常发生的机制之一。

AIM To study the changes of transient outward potassium currents （Ito） of rat myocytes after acute myocardial ischemia. METHODS Ischemia and reperfusion （I/R） model was made on rats according to the routine method. Single ventricular myocytes were isolated enzymatically from the reinfused rat hearts after 10 and 30 min myocardial ischemia respectively, Ito, was recorded by patch clamp technique in the whole cell configuration. RESULTS Ito density at ± 70 mV from cells in the reperfused hearts after 10 and 30 min ischemia were significantly reduced to 7.2 ± 2.5 pA/pF（ n = 9 ） and 6.4 ± 2.7 pA/pF （n= 10） respectively, compared with the normal control 52.2 ± 12. 1 pA/pF（n = 11）（P 〈 0.01 ）. The steady-state inactivation curve was shifted to the depolarizing direction in the reperfused after 10 and 30 min ischemla, the half-maximal voltage dependence of inactivation（ V1/2 ） was -58 ± 12 mV （ n = 8 ） in the reperfused hearts after 10 min isehemia and - 50±12 mV（ n = 9 ） （ P 〈 0.05 ） after 30 min ischemia（P 〉 0.05）. CONCLUSION Inhibitation of Ito occurs during ischemic reperfusion, which might be one of the mechanisms in the development of ventricular arrhythmias related to reperfusion after myocardial ischemia.