反复正加速度暴露及普罗帕酮干预对兔心室肌细胞复极离散度的影响

摘要

Objective To investigate the effects of repeated positive acceleration ( +Gz) exposure and propafenone intervention on transmural dispersion of repolarization ( TDR) in ventricle muscle cells of rabbits, to explore the cellular electrophysiologic mechanisms of arrhythmia induced by positive acceleration and the antagonistic mechanism of propafenone.Methods 30 male New Zealand white rabbits were randomly divided into control group, +Gz group and propafenone intervention group.The monophasic action potential ( MAP) recording technology used to record three layers of ventricular muscle cells MAP simultaneously, and to measue MAPD90 and TDR.Results Compared with the control group, the MAPD90 of endocardial and epicardial cells in +Gz group were decreased (all P<0.05), the left ventricle TDR was increased (P <0.05).Compared with the +Gz group, the MAPD90 of endocardial and epicardial cells in propafenone intervention group rabbbits were increased (all P<0.05), the left ventricle TDR was decreased (P<0.05). Conclusion The MAPD90 of ventricular muscle cells decrease and the TDR increase, maybe the cell electrophysiological mechanisms of arrhythmia induced by +Gz, and propafenone can antagonize this effect.%目的：观察反复正加速度（＋Gz）暴露及普罗帕酮干预对兔心室肌细胞跨壁复极离散度（ TDR）的影响，探讨＋Gz诱发心律失常的细胞电生理机制及普罗帕酮的拮抗机制。方法30只雄性新西兰大白兔随机均分为对照组、＋Gz组和普罗帕酮干预组。应用单相动作电位（ MAP）记录技术，同步记录左心室3层细胞MAP，测量复极达90％振幅的单相动作电位时程（ MAPD90）及跨壁复极离散度（ TDR）。结果与对照组相比，＋Gz组左心室内、外膜MAPD90均缩短，左心室TDR增大，P均＜0．05；与＋Gz组相比，普罗帕酮干预组左心室内、外膜MAPD90均增大，TDR减小，P均＜0．05。结论心室肌细胞MAPD90缩短及TDR增大，可能是＋Gz诱发快速性心律失常的细胞电生理机制；普罗帕酮可以拮抗这种改变。