缺血大鼠心肌细胞晚钠电流的变化规律和阿托伐他汀的作用  

Effects of atorvastatin on late sodium current in ventricular myocytes in rats suffering from simulated ischemia

作　　者：李小龙 万征[1] LI Xiao-long;WAN Zheng(Department of Cardiology,General Hospital,Tianjin Medical University,Tianjin 300052,China)

机构地区：[1]天津医科大学总医院心内科,天津300052

出　　处：《天津医科大学学报》2018年第4期291-293,311,共4页Journal of Tianjin Medical University

摘　　要：目的:观察不同模拟缺血时间下大鼠左室心肌细胞晚钠电流(I_(NaL))的变化规律及阿托伐他汀对该过程的作用。方法:Wistar大鼠共40只,分离左室心肌细胞,分为正常组、缺血组、正常-他汀组和缺血-他汀组。用全细胞膜片钳分别记录4组细胞基线状态下I_(NaL),再灌流3 min后,每2 min记录1次,记录10 min,观察I_(NaL)的变化规律。计算I/Imax作为标准化I_(NaL),比较4组I_(NaL)标准化值。结果:取-40 m V测试电压下,(1)正常组,基线状态和记录3、5、7、9 min 4个时间点的I_(NaL)分别为1、0.82±0.24、1.00±0.36、0.92±0.32和1.03±0.38,各记录时间点与基线之间均无差别(分别P>0.05);(2)缺血组,基线状态I_(NaL)为1,在模拟缺血3~7 min时,I_(NaL)增大,并于3 min时达峰(1.79±0.66);(3)正常-他汀组,基线状态和4个记录时间点的I_(NaL)分别为1、0.88±0.28、1.06±0.23、1.03±0.27和0.94±0.19,各记录时间点与基线之间均无差别(分别P>0.05);(4)缺血-他汀组,与基线状态相比,模拟缺血3 min时的I_(NaL)无变化,5 min时较基线值减少0.43±0.31(P=0.035),7 min时较基线值减少0.48±0.37(P=0.044);(5)在模拟缺血3 min时,相比于正常组,缺血组I_(NaL)增大(P=0.001);相比于缺血组,缺血-他汀组I_(NaL)则减小(P=0.004);正常组和缺血-他汀组的I_(NaL)之间并无差别(P>0.05)。结论:模拟缺血早期(10 min内)心室肌细胞I_(NaL)呈时间依赖性增大;5μmol/L阿托伐他汀不改变正常状态下的I_(NaL),却可抑制缺血状态下I_(NaL)的异常增大。Objective:To observe the changes of late sodium current(INaL)in left ventricular myocytes in rats suffering simulated ischemia at different time points and the effect of atorvastatin on that process.Methods:Left ventricular myocytes were isolated from forty wistar rats and randomly divided into normal group,ischemia group,normal-statin group and ischemia-statin group.Firstly,baseline INaL of all cells were recorded by whole-cell patch clamp.Secondly,cells were perfused for 3 min.Finally,INaL was recorded once every 2 min.The recording time was totally 10 min.The changes of INaL were observed.I/Imax was calculated as the standardized value of INaL.Standardized values of INaL of four groups were compared.Results:At the testing potential of-40 mV,(1)normal group,INaL of baseline and four time points was 1,0.82±0.24,1.00±0.36,0.92±0.32 and 1.03±0.38,respectively;there was no significant difference between baseline and different time points(P>0.05,respectively);(2)ischemia group,INaL of baseline was 1;INaL was increased during 3~7 min of simulated ischemia,reaching the peak at 3 min(1.79±0.66);(3)normal-statin group,INaL of baseline and four time points was 1,0.88±0.28,1.06±0.23,1.03±0.27 and 0.94±0.19,respectively;there was no significant difference between baseline and different time points(P>0.05),respectively);(4)ischemia-statin group,compared with the baseline value,INaL at 3 min of simulated ischemia didn’t change,INaL at 5 min reduced by 0.43±0.31(P=0.035),INaL at 7 min reduced by 0.48±0.37(P=0.044);(5)at 3 min of simulated ischemia:compared with normal group,INaL of ischemia group increased(P=0.001);compared with ischemia group,INaL of ischemia-statin group decreased(P=0.004),and there was no difference between normal group and ischemia-statin group(P>0.05).Conclusion:INaL of ventricular myocytes increases in a time-dependent manner at the early stage of simulated ischemia(10 min),and 5μmol/L atorvastatin dose not chang INaL in normal stagte bue could inhibit the abnoemal increase of INaL in isch

关 键 词：模拟缺血 晚钠电流 阿托伐他汀 膜片钳 

分 类 号：R331.38[医药卫生—人体生理学]