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目的:观察环维黄杨星D(Cyclovirobuxine D,CVB-D)返针晶结晶体对豚鼠单个心室肌细胞动作电位的影响。方法:使用Langendorff灌流系统离体灌流心脏,急性酶解法分离获得心肌细胞。全细胞膜片钳技术电流钳模式记录动作电位。Tyrode氏液和药物溶液交替反复灌流单个心室肌细胞。结果:CVB-D中浓度组用药后动作电位0相除极幅度(APA)从(113.3±6.3)mV下降至(110.2±6.4)mV(n=6,P<0.01),复极至50%时动作电位时程(APD50)从(616.3±68.0)ms延长至(657.4±79.5)ms(n=6,P<0.01),复极至90%时动作电位时程(APD90)从(633.5±71.2)ms延长至(669.2±74.4)ms(n=6,P<0.01),复极50%至90%动作电位时程(APD50-90)从(15.9±6.0)ms延长至(20.1±5.2)ms(n=6,P<0.01),动作电位3相复极速率(V3)从(-2.6±0.8)V/s减慢至(-2.4±0.7)V/s(n=6,P<0.01)。Tyrode氏液和高浓度药物溶液交替反复灌流后APD50-90呈递增趋势而V3呈递减趋势,其他指标的变化趋势与中浓度组一致。CVB-D低浓度组各项指标的变化趋势缺乏统计学意义。结论:体外应用CVB-D返针晶结晶体引起心室肌细胞APA减小,APD50,APD90,APD50-90延长,V3减慢。以上影响可能是其在临床上具有增强心肌收缩力和抗心律失常作用的药理机制。
Objective: To observe the effects of Cyclovirobuxine D (CVB-D) recrystallized crystals on the action potentials of single ventricular myocytes in guinea pigs. Methods: Perfused hearts were perfused with Langendorff perfusion system, and cardiomyocytes were isolated by acute enzymatic method. Whole Cell Patch Clamp Current Clamp Mode Recording Action Potential. Tyrode’s solution and drug solution were alternately perfusion of individual ventricular myocytes. Results: After treatment with CVB-D, the amplitude of APA decreased from (113.3 ± 6.3) mV to (110.2 ± 6.4) mV (n = 6, P <0.01) (APD50) increased from (616.3 ± 68.0) ms to (657.4 ± 79.5) ms (n = 6, P <0.01) (APD50-90) prolonged from (15.9 ± 6.0) ms to (20.1 ± 5.2) ms for repolarization 50% to 90% (n = 6, P <0.01). The bipolar rate of action potential decreased from -2.6 ± 0.8 V / s to -2.4 ± 0.7 V / s (n = 6, P <0.01). The concentrations of APD50-90 increased gradually while V3 decreased gradually after Tyrode’s fluid and high concentration of drug solution were repeatedly perfusion. The trend of other indexes was the same as that of medium concentration group. CVB-D low concentration group indicators of the trend of the lack of statistical significance. CONCLUSION: CVB-D recrystallization in vitro results in a decrease in APA, APD50, APD90 and APD50-90 in ventricular myocytes, and a decrease in V3. The above effect may be its pharmacological mechanism of enhancing myocardial contractility and antiarrhythmic effect in clinic.