Shen J B, Huang J, Jiang W P
Research Section of Cardiovascular Diseases, First Affiliated Hospital of Suzhou Medical College.
Zhonghua Nei Ke Za Zhi. 1992 Jul;31(7):407-9, 444.
Standard intracellular potential recording technique was used in isolated guinea pig ventricular muscle and monophasic action potential (MAP) recording technique was performed on both the epicardium and endocardium of dog hearts in vivo. The results showed that CsCl lengthened action potential durations of ventricular muscle as well as QT intervals of dog hearts. The incidence of early after depolarization (EAD) induction was 71.4%. Ventricular tachycardia induced by CsCl manifested as typical TdP in 44.4% with EAD shown on epicardial MAP recording. This suggested that EAD and triggered activity might be an important mechanism of TdP. As verapamil could depress the induction of EAD, we believe that Ca++ inward currents was responsible for the induction of EAD and TdP by CsCl.
采用标准细胞内电位记录技术记录豚鼠离体心室肌细胞动作电位，采用单相动作电位（MAP）记录技术记录犬在体心脏心外膜和心内膜的单相动作电位。结果显示，CsCl可延长心室肌动作电位时程及犬心脏QT间期。早期后除极（EAD）的诱发率为71.4%。CsCl诱发的室性心动过速在44.4%表现为典型尖端扭转型室性心动过速（TdP），心外膜MAP记录显示有EAD。这提示EAD和触发活动可能是TdP的重要机制。由于维拉帕米可抑制EAD的诱发，我们认为CsCl诱发EAD和TdP的机制与Ca++内向电流有关。
