Yang Zhao, Zhang Hong, Kong Shu, Yue Xiao-Feng, Jin Yin-Bin, Jin Jie, Huang Ye-Cho
Institute of Medical Electronics in Medical School, Key Laboratory of Biomedical Information Engineering, Ministry of Education, Xi'an Jiaotong University, Xi'an, PR China.
Physiol Meas. 2007 May;28(5):481-8. doi: 10.1088/0967-3334/28/5/003. Epub 2007 Apr 5.
Ventricular arrhythmias are commonly observed in patients with acute coronary occlusion and ischemia. The purpose of the present study is to determine ischemic electrophysiological effects and their role in ischemia-induced arrhythmia. Optical mapping of the membrane potential with voltage-sensitive dyes was used in the study. The mapping was performed with di-4-ANEPPS in Langendorff-perfused rabbit hearts. The excitation-contraction decoupler 2,3-butanedione monoxime was used to suppress motion artifacts caused by contraction of the heart. The acute global ischemia was developed by a rapid reduction of the flow rate. The experiments revealed that ischemic tissues were characterized by an obvious reduction in action potential duration and action potential upstroke, slower conduction velocity (CV) and the property of post-repolarization refractoriness. Moreover, the magnitude of CV reduced both in control and ischemia when the pacing cycle length was short. CV reduction was even early in ischemia, resulting in a broader curve during ischemia. Moreover, the dominant frequency of ventricular tachycardia/ventricular fibrillation (VT/VF) in ischemia was less than that in control, implying a decreasing tendency of VT/VF frequency for low excitability. Therefore, combined with our previous simulation study, the dynamic changes of CV and longer refractory period were suggested to play an important role in the ischemia-related arrhythmia. Low excitability in ischemic tissue was the fundamental mechanism in it.
室性心律失常常见于急性冠状动脉闭塞和缺血患者。本研究的目的是确定缺血的电生理效应及其在缺血性心律失常中的作用。本研究采用电压敏感染料对膜电位进行光学映射。映射是在Langendorff灌注兔心脏中用di-4-ANEPPS进行的。使用兴奋-收缩解偶联剂2,3-丁二酮单肟来抑制心脏收缩引起的运动伪影。通过快速降低流速来诱导急性整体缺血。实验表明,缺血组织的特征是动作电位时程和动作电位上升明显减少、传导速度(CV)减慢以及复极后不应期特性。此外,当起搏周期长度短时,对照和缺血时CV的幅度均降低。缺血时CV降低更早,导致缺血期间曲线更宽。此外,缺血时室性心动过速/心室颤动(VT/VF)的主导频率低于对照,这意味着VT/VF频率因兴奋性降低而有下降趋势。因此,结合我们之前的模拟研究,CV的动态变化和更长的不应期被认为在缺血相关心律失常中起重要作用。缺血组织中的低兴奋性是其基本机制。