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研究大鼠心室肌细胞瞬间外向钾电流(Ito1)的特性及奎尼丁对其的影响,从而从细胞离子的层面去探讨奎尼丁作为治疗Brugada综合征的侯选药物的机制。用酶解法分离大鼠单个左室细胞,应用膜片钳全细胞方法记录Ito1,观察不同浓度的奎尼丁对心室肌细胞Ito1的作用。结果:①大鼠心室肌细胞具有强大的Ito1,在0.2Hz,+70mV和32℃条件下,其平均峰值Ito1强度和密度分别为1940±440pA和12.9±2.6pA/pF;②在奎尼丁1,2.5,5,7.5,10μmol/L不同的浓度下,奎尼丁抑制Ito1程度越明显(自身对照P<0.05),其作用呈浓度依赖性。结论:奎尼丁可以通过抑制Ito1,延长动作电位的复极时程,此很有可能是其作为治疗Brugada综合征的侯选药物的机制之一。
To study the transient outward potassium current (Ito1) in rat ventricular myocytes and the effect of quinidine, and to explore the mechanism of quinidine as a candidate drug for the treatment of Brugada syndrome from the cellular ion level. Single left ventricular (LV) cells were isolated by enzymatic method and Ito1 was recorded by whole-cell patch-clamp method. The effect of different concentrations of quinidine on Ito1 in ventricular myocytes was observed. RESULTS: ① Rat ventricular myocytes had a strong Ito1, and the mean peak Ito1 intensity and density were 1940 ± 440pA and 12.9 ± 2.6pA / pF at 0.2Hz, + 70mV and 32 ℃; At different concentrations of 1, 2.5, 5, 7.5 and 10μmol / L, the effect of quinidine on Ito1 was more obvious (self-control, P <0.05), and its effect was concentration-dependent. CONCLUSION: Quinidine can prolong the repolarization duration of action potential by inhibiting Ito1, which is likely to be one of the mechanisms for its potential as a drug candidate for the treatment of Brugada syndrome.