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Abstract：
The research on the biological pacemaker has been very active in recent years. And turning nonautomatic ventricular cells into pacemaking cells is believed to hold the key to making a biological pacemaker. In the study, the inward-rectifier K+ current (I K1) is depressed to induce the automaticity of the ventricular myocyte, and then, the effects of the other membrane ion currents on the automaticity are analyzed. It is discovered that the L-type calcium current (I CaL) plays a major part in the rapid depolarization of the action potential (AP). A small enough I CaL would lead to the failure of the automaticity of the ventricular myocyte. Meanwhile, the background sodium current (I bNa), the background calcium current (I bCa), and the Na+/Ca2+ exchanger current (I NaCa) contribute significantly to the slow depolarization, indicating that these currents are the main supplementary power of the pacing induced by depressing I K1, while in the 2D simulation, we find that the weak electrical coupling plays a more important role in the driving of a biological pacemaker.
摘要：
近年来，生物起搏器的研究非常活跃。将非自动心室细胞转化为起搏细胞被认为是制造生物起搏器的关键。在研究中,抑制向内整流K电流（IK1）以诱导心室肌细胞的自动性，然后,分析了其他膜离子电流对自动性的影响。发现L型钙电流（ICaL）在动作电位（AP）的快速去极化中起主要作用。足够小的ICaL将导致心室肌细胞的自动性失败。同时,背景钠电流(IbNa)，背景钙电流(IbCa)，Na+/Ca2+交换电流(INaCa)对缓慢去极化有显著贡献，表明这些电流是通过降低IK1引起的起搏的主要补充功率，而在2D模拟中，我们发现，弱电耦合在生物起搏器的驱动中起着更重要的作用。
