银杏酮酯对模拟缺血豚鼠心室肌细胞I_K的影响

目的:观察银杏酮酯(GBE50)对模拟缺血豚鼠心室肌细胞延迟整流钾电流(IK)的影响,探讨GBE50抗心肌缺血的机制。方法:采用标准膜片钳全细胞记录方法观察GBE50对正常及模拟缺血豚鼠心室肌细胞IK的影响。结果:在细胞外液中分别加入25,50,100mg/L GBE50灌流,仅100mg/L GBE50对正常心室肌细胞IK有影响(P0.05),使IK电流密度减小,I-V曲线下移;模拟缺血液灌流20minIK减小,I-V曲线下移,在模拟缺血液中分别加入25,50,100mg/L GBE50后,仅25mg/L无效,50,100mg/LGBE50灌流20min后IK稍减小,I-V曲线稍有下移,与缺血前相比无显著性差异(P0.05)。结论:100mg/LGBE50可减少正常豚鼠心室肌细胞IK;在模拟缺血条件下豚鼠心室肌细胞IK受到明显的抑制,GBE50可明显逆转缺血所致IK的抑制效应,这可能是GBE50产生心肌保护作用的重要机制之一。

Effect of GBE50 on delayed rectifier potassium current of ventricular myocytes in ischemic guinea pig

Objective：Ginkgo biloba extract 50（GBE50） is a new multicomponent drug with a polyvalent action extracted from the leave of Ginkgo biloba. The aim of this experiment was to study the effects of GBE50 on delayed rectifier potassium current （IK） in ventricular myocytes under normal and simulated ischemia conditions in guinea pigs. Methods： Single ventricular myocytes were isolated by an enzymatic dissociation method. IK were recorded by whole-cell patch clamp technique in voltage clamp mode. GBE50 was added to the perfusion chamber from low to high concentrations（25,50,100 mg/L） in normal condition. Different concentrations of GBE50 （25,50,100 mg/L） were prepared with simulated ischemic fluid. Results： ①Under normal condition,100 mg/L GBE50 decreased IK （n=7,P0.05）. ②Under ischemia condition,it was observed that IK was inhibited （n=8,P0.05）. ③Perfusion with ischemia solution containing 50 mg/L （n=8,P0.05） and 100 mg/L GBE50 （n=6,P0.05） could reverse the decrease of IK. Conclusion： GBE50 significantly decreased IK in a concentration-dependent manner. GBE50 could alleviate the electrophysiological heterogeneity of myocardium to prevent ischemic myocardium from arrhythmia.