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目的研究海葵素-Q(AP-Q)对心室肌细胞钾电流的作用。方法采用酶解法制备豚鼠和大鼠单个心室肌单细胞,应用全细胞膜片钳记录方法记录心室肌细胞钾电流(Ito,IK和IK1)。结果AP-Q3~100nmolL-1浓度依赖性地阻滞Ito,EC50分别为10.5nmolL-1,去极化至+50mV时,AP-Q10nmolL-1使Ito从给药前的(13.3±3.4)pApF-1升至(19.46±4.3)pApF-1。AP-Q0.1~100nmolL-1浓度依赖性地增大IK和尾电流(IKtail),EC50分别为4.7和5.0nmolL-1。AP-Q1pmolL-1~100nmolL-1浓度依赖性地增大IK1,EC50值为0.2nmolL-1。结论AP-Q增大IK,Ito和IK1的作用可能是其缩短APD,增大RP的原因。
Objective To study the effect of Achillea-Q (AP-Q) on the potassium currents of ventricular myocytes. Methods The single cells of guinea pig and rat ventricular myocytes were prepared by enzymolysis, and the potassium currents (Ito, IK and IK1) of ventricular myocytes were recorded by whole-cell patch-clamp recording method. Results AP-Q10nmolL-1 blocked Ito with a concentration-dependent manner and EC50 was 10.5nmolL-1, respectively. When depolarized to + 50mV, AP-Q10nmolL-1 decreased Ito from (13.3 ± 3.4) pApF -1 to (19.46 ± 4.3) pApF-1. AP-Q 0.1 ~ 100nmolL-1 increased IK and tail current (IKtail) in a concentration-dependent manner with EC50 of 4.7 and 5.0nmolL-1, respectively. AP-Q1pmolL-1 ~ 100nmolL-1 increased IK1 in a concentration-dependent manner with an EC50 of 0.2nmolL-1. Conclusions The effect of AP-Q on IK, Ito and IK1 may be the reason for shortening APD and increasing RP.