山东医药
山東醫藥
산동의약
SHANDONG MEDICAL JOURNAL
2014年
44期
26-28
,共3页
端木鲁健%王兰%焦琳%柳百梅%孙红娇%李玉茜%于心亚%黄丛春%王俊华%罗慧兰%王建昌
耑木魯健%王蘭%焦琳%柳百梅%孫紅嬌%李玉茜%于心亞%黃叢春%王俊華%囉慧蘭%王建昌
단목로건%왕란%초림%류백매%손홍교%리옥천%우심아%황총춘%왕준화%라혜란%왕건창
正加速度%心律失常%普罗帕酮%跨壁复极离散度%单相动作电位%兔
正加速度%心律失常%普囉帕酮%跨壁複極離散度%單相動作電位%兔
정가속도%심률실상%보라파동%과벽복겁리산도%단상동작전위%토
positive acceleration%arrhythmia%propafenone%transmural dispersion of repolarization%monophasic ac-tion potential%rabbit
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。
目的：觀察反複正加速度（＋Gz）暴露及普囉帕酮榦預對兔心室肌細胞跨壁複極離散度（ TDR）的影響，探討＋Gz誘髮心律失常的細胞電生理機製及普囉帕酮的拮抗機製。方法30隻雄性新西蘭大白兔隨機均分為對照組、＋Gz組和普囉帕酮榦預組。應用單相動作電位（ MAP）記錄技術，同步記錄左心室3層細胞MAP，測量複極達90％振幅的單相動作電位時程（ MAPD90）及跨壁複極離散度（ TDR）。結果與對照組相比，＋Gz組左心室內、外膜MAPD90均縮短，左心室TDR增大，P均＜0．05；與＋Gz組相比，普囉帕酮榦預組左心室內、外膜MAPD90均增大，TDR減小，P均＜0．05。結論心室肌細胞MAPD90縮短及TDR增大，可能是＋Gz誘髮快速性心律失常的細胞電生理機製；普囉帕酮可以拮抗這種改變。
목적：관찰반복정가속도（＋Gz）폭로급보라파동간예대토심실기세포과벽복겁리산도（ TDR）적영향，탐토＋Gz유발심률실상적세포전생리궤제급보라파동적길항궤제。방법30지웅성신서란대백토수궤균분위대조조、＋Gz조화보라파동간예조。응용단상동작전위（ MAP）기록기술，동보기록좌심실3층세포MAP，측량복겁체90％진폭적단상동작전위시정（ MAPD90）급과벽복겁리산도（ TDR）。결과여대조조상비，＋Gz조좌심실내、외막MAPD90균축단，좌심실TDR증대，P균＜0．05；여＋Gz조상비，보라파동간예조좌심실내、외막MAPD90균증대，TDR감소，P균＜0．05。결론심실기세포MAPD90축단급TDR증대，가능시＋Gz유발쾌속성심률실상적세포전생리궤제；보라파동가이길항저충개변。
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.
