El-Battrawy Ibrahim, Lang Siegfried, Zhao Zhihan, Akin Ibrahim, Yücel Gökhan, Meister Sophie, Patocskai Bence, Behnes Michael, Rudic Boris, Tülümen Erol, Liebe Volker, Tiburcy Malte, Dworacek Jennifer, Zimmermann Wolfram-Hubertus, Utikal Jochen, Wieland Thomas, Borggrefe Martin, Zhou Xiao-Bo
First Department of Medicine, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany.
DZHK (German Center for Cardiovascular Research), Partner Sites, Heidelberg-Mannheim and Göttingen, Germany.
PLoS One. 2016 Nov 9;11(11):e0166143. doi: 10.1371/journal.pone.0166143. eCollection 2016.
Fever can increase the susceptibility to supraventricular and ventricular arrhythmias, in which sodium channel dysfunction has been implicated. Whether fever influences the efficacy of sodium channel blocking drugs is unknown. The current study was designed to investigate the temperature dependent effects of distinct sodium channel blocking drugs on the sodium currents in human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs).
hiPSC-CMs were generated from human skin fibroblasts of a healthy donor. The peak and late sodium currents (INa), steady-state activation, inactivation and recovery from inactivation of INa in hiPSC-CMs were analyzed using the whole-cell patch clamp technique. The effects of different concentrations of the antiarrhythmic drugs flecainide, lidocaine, ajmaline and the antianginal drug ranolazine on INa were tested at 36°C and 40°C. Increasing the temperature of the bath solution from 36°C to 40°C enhanced the inhibition of peak INa but reduced the inhibition of late INa by flecainide and lidocaine. By contrast, increasing the temperature reduced the effect of ajmaline and ranolazine on the peak INa but not late INa. None of the tested drugs showed temperature-dependent effects on the steady-state activation and inactivation as well as on the recovery from inactivation of INa in hiPSC-CMs.
Temperature variation from the physiological to the febrile range apparently influences the effects of sodium channel blockers on the sodium currents. This may influence their antiarrhythmic efficacy in patients suffering from fever.
发热会增加室上性和室性心律失常的易感性,其中钠通道功能障碍与之相关。发热是否会影响钠通道阻滞剂的疗效尚不清楚。本研究旨在探究不同钠通道阻滞剂对人诱导多能干细胞衍生心肌细胞(hiPSC-CMs)钠电流的温度依赖性影响。
hiPSC-CMs由一名健康供体的人皮肤成纤维细胞生成。使用全细胞膜片钳技术分析hiPSC-CMs中钠电流(INa)的峰值和晚期电流、INa的稳态激活、失活以及失活后恢复情况。在36°C和40°C下测试了不同浓度的抗心律失常药物氟卡尼、利多卡因、阿义马林以及抗心绞痛药物雷诺嗪对INa的影响。将浴液温度从36°C升高到40°C,增强了氟卡尼和利多卡因对INa峰值的抑制作用,但降低了对晚期INa的抑制作用。相比之下,温度升高降低了阿义马林和雷诺嗪对INa峰值的作用,但对晚期INa无影响。所测试的药物均未显示出对hiPSC-CMs中INa的稳态激活、失活以及失活后恢复有温度依赖性影响。
从生理温度到发热温度范围的变化显然会影响钠通道阻滞剂对钠电流的作用。这可能会影响它们对发热患者的抗心律失常疗效。