摘要
目的研究抗抑郁药物西酞普兰对豚鼠心脏快、慢反应动作电位和离体及在体心电图的影响,初步探讨其引起心脏不良反应的机制。方法在整体动物、离体心脏和分离的心室乳头肌标本上分别采用肢体Ⅱ导联、Langendorff灌流技术和细胞内微电极技术记录豚鼠心电图、离体心电图和心室乳头肌快、慢反应动作电位。结果西酞普兰可明显延长豚鼠心电图的RR间期,使QRS波群增宽;离体心电图显示,西酞普兰能明显减慢心率,在12.5×10-6mol/L浓度灌流下,可诱发室性早搏及房室传导阻滞。在西酞普兰作用下,豚鼠心室乳头肌快反应动作电位的0期上升速率(Vm ax)的减慢、0期上升幅值(APA)的降低和时程(APD50和APD90)的缩短呈剂量依赖性;西酞普兰可浓度依赖性抑制异丙肾上腺素所诱发的豚鼠心室乳头肌慢反应动作电位。结论西酞普兰对心脏Na+、Ca2+等离子通道具有抑制作用,此效应可能是临床应用西酞普兰时出现心律失常等不良反应的离子基础。
Objective To investigate the influence of citalopram on the fast response action potential, slow response action potential, in vitro electrocardiogram （ECG） and in vivo ECG of cardiac myocytes, and explore its mechanism of adverse cardiac effects. Methods Conventional microelectrode technique was employed to record the fast and slow response action potentials of the isolated papillary muscles of guinea pigs. In vivo and in vitro ECG were recorded from anesthetized animals and Langendorff-perfused hearts, respectively. Results Citalopram could prolong the RR interval and QRS duration of in vivo ECG. The premature ventricular contraction and atrial ventricular block were induced by 12. 5 × 10^-6 mol/L citalopram. The maximum ascending velocity of 0 phase （Vmax）, action potential amplitude （APA） and action potential duration （APD50 and APD50） were dose-dependently decreased by citalopram in the fast and slow response action potentials of guinea pigs, respectively. Conclusion Citalopram can inhibit sodium and calcium channels effectively, which may be the ionic mechanism that citalopram induces arrhythmia in the clinical practice.
出处
《上海交通大学学报（医学版）》
CAS
CSCD
北大核心
2009年第8期926-930,共5页
Journal of Shanghai Jiao tong University:Medical Science
基金
上海市科委基金(06JC14045)
上海交通大学医学院基金(2008XJ003)~~
