摘要
应用玻璃微电极技术和膜片钳全细胞记录,研究了内皮素(ET-1)致豚鼠心室肌细胞早期后除极(EADs)的作用及发生机制。结果显示:50nmo1/LET-1灌流能明显延长动作电位时程APD(50),诱发EADs。产生EADs基础可能在于促进心室肌细胞L-型钙内流(L-Ica),使稳态激活曲线左移,其作用呈浓度依赖性。
Abstract Using glass microelectrode technique and whole-cell patch clamp technique, we studied the action and mech-anism of endothelin-l (ET-1)inducing early after depolarizations(EADs) in guinea pig ventricular myocytes.The results suggested that the prolongation of APD50 was induced and EADs was demonstrated with 50 nmol/L ET-1 perfusion. These were resulted from the enhancement of L-Ica influx and a left shift on the steady-state activation curve with dose-dependence.
出处
《中华心血管病杂志》
CAS
CSCD
北大核心
1995年第5期381-383,共3页
Chinese Journal of Cardiology
基金
国家"八.五"攻关课题