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观察硫酸镁对抗乌头碱诱发的大鼠心律失常,及其对大鼠心室肌细胞钠通道电流(INa)的影响,探讨硫酸镁抗心律失常的部分离子通道机理。应用乌头碱诱发的大鼠心律失常模型,计算对照组及硫酸镁组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所用乌头碱的量;应用膜片钳全细胞记录技术,观察乌头碱、硫酸镁对大鼠心室肌细胞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,硫酸镁组所用乌头碱的量均分别显著高于对照组(31.23±6.95μgvs24.67±5.25μg;45.00±7.93μgvs28.15±6.26μg;82.73±10.31μgvs75.47±11.26μg)。利用膜片钳技术观察到对照组、乌头碱组及硫酸镁组INa密度分别为:90.57±11.25pA/pF,98.31±26.63pA/pF,73.10±14.25pA/pF,3组数据,两两比较,差异均有显著性,P均<0.05。乌头碱组及硫酸镁组INa的IV曲线分别向下方及上方移位。结论:硫酸镁能够对抗乌头碱诱发的大鼠心律失常,其机理之一与它能够阻断I有关。
To observe the effect of magnesium sulfate on aconitine-induced arrhythmia in rats and its effect on sodium channel current (INa) in rat ventricular myocytes, and to explore the mechanism of partial ion channel of anti-arrhythmia of magnesium sulfate. Application of aconitine-induced rat arrhythmia model to calculate the control group and magnesium sulfate group induced ventricular premature beats, ventricular tachycardia / ventricular fibrillation and cardioplegia with the amount of aconitine; patch clamp Whole-cell recording technique was used to observe the effect of aconitine and magnesium sulfate on INa in rat ventricular myocytes. Results: The amount of aconitine in the magnesium sulfate group was significantly higher than that in the control group (31.23 ± 6.95μg vs 24.67 ± 5.25μg, p <0.05) when induced premature ventricular premature ventricular contraction, ventricular tachyarrhythmias / ventricular fibrillation and cardiac arrest ; 45.00 ± 7.93 μg vs 28.15 ± 6.26 μg; 82.73 ± 10.31 μg vs 75.47 ± 11.26 μg). The patch-clamp technique was used to observe the INa densities of the control group, the aconitine group and the magnesium sulfate group: 90.57 ± 11.25pA / pF, 98.31 ± 26.63pA / pF, 73.10 ± 14.25pA / pF, Comparison, the difference was significant, P <0.05. The IV curves of INa in aconitine group and magnesium sulfate group shifted downward and upward, respectively. CONCLUSIONS: Magnesium sulphate is able to counteract aconitine-induced arrhythmia in rats and one of its mechanisms is related to its ability to block I.