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目的:观察银杏酮酯(GBE50)对心肌生理特性及细胞内游离钙的影响,探讨GBE50抗心律失常的机制。方法:采用常规离体器官实验法记录心房生理特性,激光共聚焦显微技术测定细胞内游离钙。结果:银杏酮酯各组(10,20,40,80,160 mg.L-1)对右心房收缩频率抑制率,除10 mg.L-1外,其他各组与对照组比较均具有显著性差异(P<0.05或P<0.01)。各组对右心房收缩力与对照组比较均具有显著性差异(P<0.05)。各组对左心房收缩力抑制率与对照组比较均具有显著性差异(P<0.05或P<0.01)。各组对左心房静息后增强效应与对照组比较均具有显著性差异(P<0.05或P<0.01)。40,80,160 mg.L-1的GBE50对左心房功能不应期呈延长效应(P<0.01);50 mg.L-1GBE50灌流后4,8,12 min心室肌细胞内[Ca2+]i比灌流前减少(P<0.01)。结论:银杏酮酯可降低右心房自律性,降低心房收缩力;延长左心房功能不应期(FRP),降低左心房的静息后增强效应的作用,且作用呈一定剂量依赖性。这些作用可能与减少心室肌细胞内游离钙浓度有关。
Objective: To observe the effect of ginkgo ketoester (GBE50) on myocardial physiological characteristics and intracellular free calcium, and to explore the mechanism of GBE50 anti-arrhythmia. METHODS: The physiological characteristics of atrial tissue were recorded by routine isolated organ test and intracellular free calcium was determined by laser confocal microscopy. RESULTS: The inhibition rate of right atrial contraction frequency in each group (10, 20, 40, 80, 160 mg.L-1) of Ginkgo biloba extract was significantly different from that of the control group except 10 mg.L-1. (P<0.05 or P<0.01). There was a significant difference in the right atrial contractility between the groups and the control group (P<0.05). The inhibition rate of left atrial contraction force of each group was significantly different from that of the control group (P<0.05 or P<0.01). There was a significant difference between the left atrial resting enhancement effect and the control group (P<0.05 or P<0.01). GBE50 of 40, 80, 160 mg.L-1 showed a prolonged effect on left atrial function refractory period (P<0.01); intracellular [Ca2+]i ratio of ventricular myocytes was increased at 4, 8, and 12 min after 50 mg.L-1 GBE50 perfusion. The former decreased (P<0.01). Conclusion: Ginkgo Biloba extract can reduce right atrial self-discipline, reduce atrial contractility; prolong the left atrial function refractory period (FRP) and reduce the left atrial resting after the enhancement effect, and the effect is dose-dependent. These effects may be related to the reduction of intracellular free calcium concentration in ventricular myocytes.