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本实验通过结扎兔冠状动脉左室支复制动物缺血—再灌注模型,应用心外膜接触电极记录单相动作电位(MAP),观察后除极电位在再灌注性心律失常中作用及镁离子的拮抗作用。结果表明,再灌注性心律失常(RA)的52.6％(10/19)与早期后去极化(EAD)有关。硫酸镁可终止及预防RA,对再灌中出现触发活动有抑制作用。硫酸镁用药后使再灌心脏降低的单相动作电位振幅(MAPA)升高,改善缺血区及缺血边缘区的复极离散度(△APD)。结果显示,镁对再灌注心肌电生理有良好的保护作用。
In this study, the model of ischemia-reperfusion injury was established by ligation of left ventricular branches in rabbit coronary arteries. Single-phase action potential (MAP) was recorded by epicardial contact electrodes. The effects of depolarization potentials on reperfusion arrhythmias and magnesium ions Antagonism. The results showed that 52.6% (10/19) of reperfusion arrhythmias (RA) were associated with early post-depolarization (EAD). Magnesium sulfate can be terminated and prevent RA, triggering activities in reperfusion have an inhibitory effect. After administration of magnesium sulfate, the single-phase action potential amplitude (MAPA) decreased and the repolarization dispersion (△ APD) in the ischemic and ischemic marginal areas improved after reperfusion. The results show that magnesium has a good protective effect on myocardial electrophysiology after reperfusion.