Involvement of the persistent Na+ current in the diastolic depolarization and automaticity of the guinea pig pulmonary vein myocardium
Involvement of the persistent Na+ current in the diastolic depolarization and automaticity of the guinea pig pulmonary vein myocardium
复制标题
持续Na电流参与豚鼠肺静脉心肌舒张期除极和自律性
DOI：
10.1016/j.jphs.2019.08.003
复制
发表时间：
2019
影响因子：
3.5
通讯作者：
Tanaka Hikaru
中科院分区：
文献类型：
--
作者：
Irie Masahiko;Hiiro Haruhito;Hamaguchi Shogo;Namekata Iyuki;Tanaka Hikaru
在豚鼠肺静脉心肌细胞和组织标本上，观察了Na+电流在肺静脉心肌自律性中的作用。河豚毒素通过抑制动作电位的舒张期去极化而抑制肺静脉组织制备的自律性。ATX-II增加Na+电流持续成分的密度(晚期INa)，引起静息膜电位的去极化，进而引起动作电位的自发放电。抑制晚期INA的GS-458967可抑制舒张期去极化和动作电位的放电。Pilsicainide仅抑制Na+电流的瞬时成分(INa峰)，对放电频率无影响。GS-458967对工作心肌的收缩力无影响。结论：晚期INAI参与了肺静脉心肌舒张期去极化和自律性。晚期异丙肾上腺素抑制剂似乎是治疗房颤的有效药物，对工作心肌的不良影响最小。
The role of the Na+current in the automaticity of the pulmonary vein myocardium was examined in isolated guinea pig pulmonary vein cardiomyocytes and tissue preparations. Tetrodotoxin inhibited the automaticity of pulmonary vein tissue preparations by suppressing the diastolic depolarization of the action potential. ATX-II, which increased the density of persistent component of the Na+current (late INa), induced a depolarization of the resting membrane potential followed by spontaneous firing of action potentials. GS-458967, which inhibited the late INa, suppressed the diastolic depolarization and the firing of action potentials. Pilsicainide, which inhibited only the transient component of Na+current (peak INa), had no effect on the firing frequency. GS-458967 had no effect on the contractile force of the working myocardium. In conclusion, late INais involved in the diastolic depolarization and automaticity of the pulmonary vein myocardium. Late INainhibitors appear to be effective therapeutic agents for atrial fibrillation with minimum adverse effects on the working myocardium.