中文摘要：

目的研究丹参酮Ⅱ对乳鼠窦房结细胞快激活延迟整流钾电流（IKr）的作用。方法选择新生24h内Wistar大鼠乳鼠，分离、培养乳鼠窦房结细胞，运用全细胞膜片钳技术记录IKr，采用细胞外灌流的方法应用丹参酮Ⅱ，观察其对IKr电流的影响。结果30μmol／L丹参酮Ⅱ可以使乳鼠窦房结细胞搏动频率显著加快，从（157．2±10．3）次／min增加至（268．1±12．6）次／min。30μmol／L丹参酮Ⅱ使IKr的尾电流（IKr,tail）电流密度从（54．6±4．7）pA／pF增加至（86．3±8．3）pA／pF（P〈0．01）。在1～100μmol／L范围内，此作用呈浓度依赖性特征，半数有效浓度（EC50）为（29．3±1．02）μmol／L，Hill系数为1．05.门控机制研究发现，该效应与药物增加乳鼠窦房结细胞IKr的激活和失活后恢复有关，而与通道失活关系不大。结论丹参酮Ⅱ可以增加乳鼠窦房结细胞IKr的电流密度，从而缩短复极时间，增加搏动频率。

英文摘要：

Objective To investigate the effects of sodium tanshinone Ⅱ A sulfonate （STS） on rapidly activating component of delayed rectifier K current （IKr） in sinoatrial node cells （SNCs） from neonatal rats. Methods The SNCs were isolated and cultured from the sinus node tissues derived from neonatal rats （ 〈 24 hours old） by enzymatic dispersion with differential attachment as well as 5＇-bromodeoxyufidine （5-BrdU）. IKr currents in the STS treated cells were measured by whole-cell configuration with patch-clamp technique. Results The frequency of SNCs beat was significantly increased by 30μmol/L STS, from （157.2 ± 10.3） to （268.1 ± 12.6） times/min. This dose of STS induced the current densities of IKr,tail increased from （54.6 ±4.7） to （86.3 ± 8.3） pA/pF （n = 10, P〈 0.01）. IKr,tait was excited by 1 to 100μmol/L STS in a dose-dependent fashion, with a half maximal effective concentration （EC50） of （29.3 ± 1.02）μmol/L and Hill coefficient of 1.05. Investigation of gating mechanism showed that the effect was associated with the increase of STS concentration enhancing the steady-state activation and the recovery of inactivation of IKr,tail currents in SNCs, but hade little effect on the steady-state inactivation of/Hr. Conclusion STS improves the densities of IKr, and then shortens repolarization duration and enhances pulse frequency of SNCs.