论文部分内容阅读
目的对比研究正常和缺血心肌在正加速度(+Gz)暴露下动作电位的变化,探讨心肌在冠脉病变所致缺血基础上发生心律失常的可能机制。方法新西兰大白兔60只,随机分为对照组(A组)、加速度组(B组)、缺血组(C组)、缺血+加速度组(D组),每组15只。采用单向动作电位法,记录并对比分析各组动物心肌缺血、+Gz暴露后单相动作电位振幅(MAPA)、0相最大上升速率(Vmax)、复极达50%振幅的单相动作电位时程(MAPD50)、复极达90%振幅的单相动作电位时程(MAPD90)的变化;记录完动作电位后再行S1S1程序刺激,观察心律失常诱发率。结果各组间MAPA和Vmax均无明显变化(P>0.05);与A组比较,B、C、D组MAPD50和MAPD90均明显缩短(P<0.05),其中D组较B、C组缩短程度大(P<0.05)。B、C、D组心律失常诱发率均明显高于A组(P<0.05),且D组明显高于B、C组(P<0.05)。结论 +Gz或缺血暴露后心肌细胞动作电位时程缩短,心律失常诱发率增加,且两因素之间有叠加效应,提示复极过程中存在相关离子通道功能异常。
Objective To compare the changes of action potentials of normal and ischemic myocardium under positive acceleration (+ Gz) exposure and to explore the possible mechanism of myocardial arrhythmia on the basis of ischemia induced by coronary lesions. Methods Sixty New Zealand white rabbits were randomly divided into control group (A group), acceleration group (B group), ischemia group (C group), ischemia + acceleration group (D group) The single-phase action potential method was used to record and compare the single-phase action amplitude (MAPmax), maximum phase velocity (Vmax) of 0 phase and maximum amplitude of 50% (MAPD50) and 90% amplitude of bipolar voltage (MAPD90). After recording the action potentials, the S1S1 program was used to stimulate and observe the induction rate of arrhythmia. Results Compared with group A, the MAPD50 and MAPD90 of group B, C and D were significantly shortened (P <0.05), and there was no significant difference between group B and group C (P> 0.05) Large (P <0.05). The induced rates of arrhythmia in groups B, C and D were significantly higher than those in group A (P <0.05), and the rates in group D were significantly higher than those in groups B and C (P <0.05). Conclusions After + Gz or ischemia exposure, the duration of action potential of cardiomyocytes is shortened and the induced rate of arrhythmia is increased, and there is a superposition effect between the two factors, suggesting the dysfunction of related ion channels in repolarization.