低温缺血再灌注大鼠心房肌电生理变化:离体实验  

Electrophysiological changes of atrial myocardium in a rat model of hypothermic ischemia-reperfusion:an in vitro experiment

作　　者：何幼芹 王贵龙 高鸿 刘艳秋 李华宇 冯玉蓉 苏殿三[4] 唐剑 He Youqin;Wang Guilong;Gao Hong;Liu Yanqiu;Li Huayu;Feng Yurong;Su Diansan;Tang Jian(School of Anesthesiology,Guizhou Medical University,Guiyang 550004,China;The Third Affiliated Hospital of Guizhou Medical University,Duyun 558000,China;Department of Anesthesiology,Affiliated Hospital of Guizhou Medical University,Guizhou 550004,China;Department of Anesthesiology,Renji Hospital,Shanghai Jiaotong University School of Medicine,Shanghai 200127,China)

机构地区：[1]贵州医科大学麻醉学院,贵阳550004 [2]贵州医科大学第三附属医院,都匀558000 [3]贵州医科大学附属医院麻醉科,贵阳550004 [4]上海交通大学医学院附属仁济医院麻醉科,200127

出　　处：《中华麻醉学杂志》2019年第9期1081-1084,共4页Chinese Journal of Anesthesiology

摘　　要：目的评价低温缺血再灌注大鼠心房肌电生理变化。方法取成功建立Langendorff离体灌注模型的SD大鼠心脏16个,采用随机数字表法分为对照组(C组)和低温缺血再灌注组(IR组),每组8个。根据是否发生房性心律失常将IR组分为再灌注非房性心律失常亚组(R-NAA组)和再灌注房性心律失常亚组(R-AA组)。C组:37℃K-H液平衡灌注120 min;IR组:37℃K-H液平衡灌注30 min后停止,注射Thomas液(4℃,20 ml/kg)使心脏停搏60 min,心脏周围用低温(4℃)Thomas液保护,停搏30 min时复灌4℃Thomas液(10 ml/kg),停搏60 min时复灌37℃K-H液30 min。于平衡灌注30 min(T0)、平衡灌注105 min/再灌注15 min(T1)和平衡灌注120 min/再灌注30 min(T2)时记录右心房单相动作电位,测量0相最大上升速率(Vmax)、单相动作电位振幅(MAPA)、单相动作电位复极50%和90%的时程(MAPD50和MAPD90)。于T2时记录心房有效不应期(ERP)和右心房传导速度(CV),计算ERP与MAPD90比值(ERP/MAPD90);行程控增频电刺激诱发房颤,记录诱发房颤的最大起搏周长(AF-PCLmax)。结果与C组和R-NAA组比较,R-AA组T1时Vmax降低、MAPD90增加,T2时CV和ERP/MAPD90降低,MAPD90、ERP和AF-PCLmax增加(P<0.05)。结论除极速度减慢、复极时程延长及传导速度、兴奋性和电稳定性降低可能是大鼠再灌注房性心律失常的电生理机制。Objective To evaluate the electrophysiological changes of atrial myocardium in a rat model of hypothermic ischemia-reperfusion(I/R).Methods Sixteen isolated Sprague-Dawley rat hearts successfully perfused in the Langendorff apparatus were divided into control group(group C)and hypothermic I/R group(group IR)using a random number table method,with 8 heats in each group.Heats in group IR were further divided into reperfusion-non-atrial arrhythmia subgroup(group R-NAA)and reperfusion-atrial arrhythmia subgroup(group R-AA)depending on whether atrial arrhythmia occurred after reperfusion.In group C,the heart was perfused with K-H solution at 37℃for 120 min.In group IR,the heart was perfused with K-H solution at 37℃for 30 min and then perfusion was stopped,cardiac arrest was induced for 60 min through injecting Thomas solution(4℃,20 ml/kg),the area around the heart was protected with low temperature(4℃)Thomas solution,and hearts were resuscitated with 4℃Thomas solution(10 ml/kg)at 30 min after cardiac arrest and with 37℃K-H solution for 30 min staring from 60 min after cardiac arrest.At 30 min of equilibration(T0),105 min of equilibration/15 min of reperfusion(T1),and 120 min of equilibration/30 min of reperfusion(T2),right atrial monophasic action potentials,maximal velocity of phase zero,monophasic action potential amplitude(MAPA)and MAP duration at 50%and 90%of repolarization(MAPD50 and MAPD90)were measured.Right-atrium conduction velocity and effective refractory period were recorded at T2,and the ratio of ERP to MAPD90(ERP/MAPD90)was calculated.Atrial fibrillation was induced by programmed electrical stimulation,and the maximum pacing cycle length of inducing atrial fibrillation(AF-PCLmax)was recorded.Results Compared with C and R-NAA groups,the maximal velocity of phase zero was significantly decreased and MAPD90 was increased at T1,the right-atrium conduction velocity and ERP/MAPD90 ratio were decreased and MAPD90,effective refractory period and AF-PCLmax were increased at T2 in group R-AA(P<0.05).Co

关 键 词：心肌再灌注损伤 心律失常 心性 心房 

分 类 号：R614[医药卫生—麻醉学]