应用心内膜单相动作电位对兔在体心脏触发性心律失常的实验研究

An experimental study on endocardial monophasic action potentials and triggered arrhythmias in rabbit heart in vivo

为探讨触发性心律失常的发生机制和诊疗依据，应用接触电极记录心内膜单相动作电位（ＭＡＰ），研究维拉帕米、美多洛尔、三磷酸腺苷（ＡＴＰ）等对氯化铯（ＣｓＣｌ）诱出兔在体心脏触发活动的影响。结果表明：（１）维拉帕米对ＣｓＣｌ诱发触发活动既能干预形成，又能对抗、终止，提示ＣｓＣｌ致触发活动与Ｃａ２＋密切相关，Ｃａ２＋转运异常可能是后除极形成的机制；（２）美托洛尔难以阻止ＣｓＣｌ诱发触发活动的形成，提示交感神经参与触发活动的作用是有限的；（３）ＡＴＰ能有效抑制ＣｓＣｌ诱发的早期后除极（ＥＡＤ），而对其诱发延迟后除极（ＤＡＤ）具有双重作用，即对ＤＡＤ先有短暂促进，继而迅速抑制。研究表明，ＭＡＰ技术对研究兔在体心脏触发活动具有重要意义。

The goal of this study was to investigate the mechanism, diagnosis and treatment of triggered arrhythmias. The impacts of verapamil, metoprolol and adenosine thiphosphate (ATP) on triggered activities induced by cesium chloride (CsCl) were elucidated by using monophasic action potentials in rabbit heart in vivo . The results showed that verapamil could not only prevent CsCl induced triggered arrhythmias but also terminate it, which suggested that CsCl induced triggered activity was related to Ca 2+ closely and the abnormal calcium transport was probably involved in the mechanisms of induced early after depolarization. The fact that metoprolol could hardly terminate CsCl induced triggered arrhythmias indicated the limited effect of sympathetic nervous tension on triggered activity. Furthermore, ATP could abolish the early after depolarization induced by CsCl and had biphasic effect on delayed after depolarization. In conclusion, monophasic action potential is valuable in studying triggered activity in vivo .