硫酸镁抗实验性心律失常及其对钠电流的影响

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。

Antiarrhythmic Effects of Magnesium Sulfate on Experimental Arrhythmias and Its Influences on INa in Rats Ventricular Cells

To observe the antiarrhythmic effects of magnesium sulfate on aconitine-induced arrhythmias in rats and its influences on I_ Na in rats ventricular cells,aconitine-induced arrhythmias model in rats were used. The doses of aconitine to induce ventricular premature beat(VPB), ventricular tachycardia(VT)/ ventricular fibrillation(VF), and cardiac arrest(CA) were contrasted in control group and magnesium group, respectively. Rat cardiomyocytes were dissociated with collagenase to acquire single ventricular myocytes. Sodium channel currents(I_ Na) were recorded using whole-cell recording patch clamp technique. The influences of aconitine and magnesium sulfate on I_ Na were studied. Results: The doses of aconitine to produce VPB, VT/VF, and CA were significantly larger in control group than in magnesium group: 31.23±6.95 μg vs 24.67±5.25 μg; 45.00±7.93 μg vs 28.15±6.26 μg; 82.73±10.31 μg vs 75.47±11.26 μg; respectively. I_ Na current density were 90.57±11.25 pA/pF, 98.31±26.63 pA/pF, 73.10±14.25 pA/pF in control group, aconitine group and magnesium group, respectively. The date was significantly different in the three groups(P<0.05). The Current-voltage(I-V) curve was shifted to downward and upward respectively in aconitine group and in magnesium group. Conclusion: Magnesium sulfate has antiarrhythmic effects on aconitine-induced arrhythmias in rats. One mechanism of its antiarrhythmic effects is related to inhibition of sodium channel current.