摘要
本实验在培养的鼠心肌细胞上观察到:在无钡培养基中,心肌细胞可因膜超极化而使动作电位发放及自发性搏动停止;向培养基中加入0.1mMBaCl_2所致的除极化足以使此停搏的心肌细胞群落恢复搏动,并能使非搏动群落转化为搏动群落。当培养基中BaCl_2浓度在0.3—4.8mM范围内递增时,呈现剂量依赖性的搏动频率加快;动作电位的APA、OS、MDP、TP递减;APDbp、APDth、F递增,显著性由P<0.05递增至P<0.001。当BaCl_2浓度高于4.8mM时,又可因过度除极化而使动作电位及搏动骤停。上述实验所见完全符合钡离子阻塞钾通道,并可经钙通道内流、启动收缩的基本机制。
The following events were observed in this experiment: Owing to the hyperpolarization of membrane, when the cardiac cells exposed to medium without barium, the discharge of action potential and beating might be stopped. The depolarization of membrane induced by 0.1 mM BaCl_2 was effective enough to restore the spontaneous contractility of those clusters which had stopped beating in medium without barium and converse the unbeating clusters into beating clusters. When the concentration of BaCl_2 in culture medium was increased step by step from 0.3-4.8 mM, dosage-dependently the beating rate increased and the action potential varied—APA, OS, MDP, TP decreased while APDbp, APDth and F increased (P<0.05-P<0.001). When the concentration of BaCl_2 was more than 4.8mM, the discharge of action potential and beating could be stopped suddenly because of severe depolarization.
The above results were consistent with basic mechanism of that barium ions are able to plug K channel, pass through Ca channel and initiate contraction.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1991年第3期310-313,共4页
Chinese Journal of Pathophysiology
关键词
心肌细胞
培养
动作电位
钡
Barium
Action potehtial
Cells, cultured
Myocardium
