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机构地区:[1]武汉科技大学医学院心脏电生理研究室,湖北武汉430080
出 处:《中国病理生理杂志》2005年第12期2490-2493,共4页Chinese Journal of Pathophysiology
基 金:湖北省自然科学基金资助项目(NO.2003ABAL89);湖北省教育厅科学基金资助项目(NO.2002A01101)
摘 要:Patalak等(1986)首次从单通道水平在蛙骨骼肌细胞发现有持续性钠电流(INa.p)存在(也称晚钠电流,INa.L),即在电压除极钳制后很长的几百毫秒时间内,仍可见到钠通道的活动.INa.p失活缓慢,参与维持动作电位的平台期,对起搏电流有一定作用,存在跨心室壁分布弥散[1,2].对持续性钠电流本质的认识大多数研究支持其是短暂钠电流通道失活机制的修饰或丧失[3].近年来对INa.p与临床病理生理过程和疾病的关系的研究有了较大进展,本文拟就这些方面作一综述.A persistent sodium current (INa.p) in ventrieular myocytes is produced hy the sodium channel activity afiler the transient sodium cun'ent. Most studies suggest that the essence of persistent sodium current is produced by the modification of inactivation gate of transient current channel or the loss of this gate. The persistent so,hum current, which inactivation is slow, contributes to the plateau period of action potential and pacemaking current. Its distribution density is different across the ventricular wall. The investigation suggests that INa.p is regulated by the oxygen sensor on membrane, action of nitric oxide or β- subunit and so on. Hypoxia increases the persistent sodium current, which plays a significant role in early afterpolarization and an-hythmogenesis in some pathological conditions and inherited disease. The role of persistent sodium current in heart failure is still full of argnmentation. Persistent sodium current and transient sodium current exist in different reaction to some regents. The above results indicate that it is significant to acknowledge the disturbance of clinical electrophysiology through investigating change and mechanisms of INa.p. Morever, as a novel target of anti - arrhythmias drugs, this current should be paid more attention.
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