利多卡因和维拉帕米对心肌缺血-再灌注性心律失常及血流动力学的干预作用

Intervention of myocardial ischemia-reperfusion arrhythmia and hemodynamics with lidocaine and verapamil

目的:探讨利多卡因和维拉帕米对在体SD大鼠心肌缺血-再灌注性心律失常(RA)及血流动力学的干预作用.方法:SD大鼠48只随机分为4组:假手术组,生理盐水(1.0mL/kg)处理组,利多卡因(10.0mg/kg)处理组,维拉帕米(2.0mg/kg)处理组.用丝线阻断左冠状动脉中段20min,在再灌注前2min经静脉分别给予生理盐水、利多卡因或维拉帕米.松开丝线实现再灌注20min.记录实验全过程中动物的左室收缩(舒张)压(LVSP/LVDP)、压力/时间微分(±dp/dt)以及标Ⅱ导联心电图.结果:比较再灌注20min后(30min)与再灌注开始时(10min),药物干预对于LVSP和±dp/dtmax的影响具有统计学意义(P<0.05,P<0.05,P<0.01);而对LVDP的影响无统计学意义;药物干预对于QRS波群时程(DQRS)和ST段抬高平均值(MST)的影响具有统计学意义;药物干预对于HR和PRI的影响具有统计学意义(P<0.01,P<0.01).结论:用利多卡因和维拉帕米对RA进行干预时,具有一定的抗心律失常和减少心肌耗氧量的作用:利多卡因可显著缩短DQRS,维拉帕米可显著减轻ST段抬高,并可减慢心率、减少心肌耗氧量;但是两者对心肌功能均有较大的影响,易造成血流动力学的紊乱.

AIM： To investigate intervention of in vivo myocardi- al ischemia-reperfusion arrhythmia （RA） and hemodynamics with lidocaine and verapamil in SD rats. METHODS： SD rats were randomly divided into 4 groups ： sham group, normal saline group （1.0 mL/kg）, lidocaine group （10.0 mg/kg） and verapamil group （2.0 mg/kg）. Middle segment of Left coronary artery was occluded with silk suture for 20 min and 2 min prior to reperfusion, normal saline, lidocaine or verapamil was administered iv. Suture was loosened to achieve reperfusion and left ventricular systolic/diastolic pressure （LVSP/LVDP）, ＋ dp/dt and ECG Ⅱ were continuously recorded. RESULTS： Comparison between 20 min after reperfusion and the onset of reperfusion revealed that the treatment intervened LVSP and ＋ dp/dtm= in a statistically significant manner （ P 〈 0.05, P 〈 0.05, P 〈 0.01 ） but inter- vened LVDP in a statistically non-significant manner （ P 〉 0.05 ）. The treatment intervened the duration of QRS wave （P 〈 0.01 ）, the mean of ST segment elevation （MST） （P 〈0.01 ）, the heart rate（P 〈0.01 ） and the pressure-rate index（P 〈0.01 ） in a statis- tically significant manner. CONCLUSION： Intervention of RA with lidocaine and verapamil achieves substantial arrhythmic effects and decreases the myocardial consumption of oxygen. Lidocaine shortens DQRS significantly while verapamil significantly alleviates the ST segment elevation and slows the heat rate to decrease myocardial consumption of oxygen. However, both agents are liable to interfere with cardiac function and further result in an imbalance of hemodynamics.