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评价卡维地洛抗大鼠实验性心律失常的作用 ,探讨其抗心律失常作用的离子通道机理 ,为临床用药提供理论依据。采用乌头碱诱发大鼠心律失常模型 ;采用膜片钳技术 ,观察乌头碱、卡维地洛对急性分离的大鼠心室肌细胞钠通道电流 (INa)的影响。结果 :诱发大鼠出现室性早搏、室性心动过速、心室颤动及心脏停搏时 ,对照组及卡维地洛组所用乌头碱的量 (μg)分别为 :室性早搏 :2 1.75± 3.4 7vs 31.81± 2 .0 4 ;室性心动过速 :2 3.5 2± 4 .13vs 36 .0 6± 3.79;心室颤动 :37.6 3± 7.94vs 6 4 .13± 1.4 0 ;心脏停搏 :6 9.31± 1.85vs 84 .6 5± 5 .2 5。利用膜片钳技术观察到 :对照组INa密度为 :5 8.6 3± 11.6 5 pA/pF ;卡维地洛组加入乌头碱后以及再加入卡维地洛后的INa密度分别为73.35± 12 .80 (pA/pF) ;10 .19± 0 .0 2 (pA/pF) ,与自身加药前相比P <0 .0 5。乌头碱及卡维地洛使INaI V曲线分别向下方及向上方移位。结论 :卡维地洛具有抗乌头碱诱发的大鼠心律失常的作用 ,其抗心律失常作用机制之一可能与Ⅰ类抗心律失常药类似 ,即抑制INa。
To evaluate the effect of carvedilol on experimental arrhythmia in rats and to explore its mechanism of anti-arrhythmic ion channel, providing a theoretical basis for clinical use. The rat model of arrhythmia was induced by aconitine. The effects of aconitine and carvedilol on the sodium channel current (INa) of acutely isolated rat ventricular myocytes were observed by patch-clamp technique. Results: The amount of aconitine (μg) used in the control group and the carvedilol group when induced premature ventricular premature ventricular tachycardia, ventricular tachycardia, ventricular fibrillation and cardiac arrest were as follows: premature ventricular contractions: 1.75 ± 3.4 7 vs 31.81 ± 2.04; Ventricular Tachycardia: 2 3.5 2 ± 4 .13 vs 36 .0 6 ± 3.79; Ventricular Fibrillation: 37.6 3 ± 7.94 vs 6 4 .13 ± 1.4 0; Cardiac Arrest: 6 9.31 ± 1.85 vs 84 .6 5 ± 5 .2 5. The patch-clamp technique was used to observe the INa density of control group: 5 8.6 3 ± 11.6 5 pA / pF; the INa densities of carvedilol group after adding aconitine and re-adding carvedilol were 73.35 ± 12 .80 (pA / pF); 10.19 ± 0.022 (pA / pF), P <0. 05 compared with that before administration. The aconitine and carvedilol shifted the INaI V curve downward and upward, respectively. CONCLUSION: Carvedilol has the anti-aconitine-induced arrhythmia in rats. One of its anti-arrhythmic mechanisms may be similar to class I anti-arrhythmic drugs, namely INa.