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目的:观察苦参碱对豚鼠心室肌细胞钠离子通道电流(I Na)的影响,探讨其抗心律失常的作用机制。方法:豚鼠随机分为正常对照组、乌头碱组和苦参碱组。每组8只。乌头碱组以50μmol·L-1乌头碱灌流10 min,苦参碱组在乌头碱组基础上,以10,50,100μmol·L-1苦参碱灌流20 min。采用膜片钳全细胞记录技术记录豚鼠单个心肌细胞钠电流并绘制电流密度电流强度(PA)/细胞膜电容(pF)曲线。结果:50μmol·L-1乌头碱显著增大I Na(-92.62±6.5)pA/pF[和对照组比较(-66.24±4.8)pA/pF,P<0.05]。在乌头碱灌流基础上,10μmol·L-1苦参碱对I Na没有明显作用,50μmol·L-1可使I Na减小至(-49.21±5.1)pA/pF(和乌头碱组比较P<0.05),100μmol·L-1又使I Na稍微增大(和对照组比较P>0.05)。结论:苦参碱抑制I Na电流,呈浓度依赖性,浓度较高时抑制I Na电流作用减弱,表现为双向调节的药理作用,可能是苦参碱抗心律失常作用温和持久的机制之一。
Objective: To observe the effect of matrine on sodium ion channel current (I Na) in guinea pig ventricular myocytes and to explore its anti-arrhythmic mechanism. Methods: Guinea pigs were randomly divided into normal control group, aconitine group and matrine group. Each group of 8. Aconitine group with 50μmol·L-1 aconitine perfusion for 10 min, matrine group aconitine group, 10,50,100μmol·L-1 matrine perfusion for 20 min. Patch clamp whole-cell recording technique was used to record the sodium currents in guinea pig single myocytes and the current density (PA) / membrane capacitance (pF) curves were plotted. Results: 50 μmol·L-1 aconitine significantly increased I Na (-92.62 ± 6.5) pA / pF compared with control group (-66.24 ± 4.8) pA / pF, P <0.05]. On the basis of aconitine perfusion, 10μmol·L-1 matrine had no significant effect on I Na, and 50μmol·L-1 reduced I Na to (-49.21 ± 5.1) pA / pF Compared with P <0.05), 100μmol·L-1 increased I Na slightly (P> 0.05 compared with the control group). CONCLUSION: Matrine inhibits I Na current in a concentration-dependent manner. When the concentration of matrine is decreased, the inhibitory effect of I Na current is weakened, showing a pharmacological effect of bidirectional regulation. It may be one of the mechanisms of matrine’s anti-arrhythmic action.