机构地区:[1]织金县人民医院麻醉科,贵州省毕节市552100 [2]贵州医科大学第三附属医院麻醉科 [3]贵阳市第四人民医院麻醉科 [4]贵州医科大学麻醉学院
出 处:《临床麻醉学杂志》2020年第5期468-472,共5页Journal of Clinical Anesthesiology
摘 要:目的观察七氟醚对低温全心缺血-再灌注心律失常心肌组织Kir2.1蛋白表达的影响。方法健康成年雄性SD大鼠,体重280~320 g,制备Langendorff离体心脏灌注模型24只,K-H液平衡灌流15 min后,随机分为三组:对照组(C组)、低温全心缺血-再灌注组(IR组)和七氟醚组(Sev组),每组8只。C组持续平衡灌流37℃K-H液105 min。IR组K-H液继续灌流15 min后,采用4℃Thomas液20 ml/kg使心脏停跳60 min,心脏周围用4℃的Thomas液进行保护,在心脏停跳30 min时追加注射4℃Thomas液10 ml/kg,在心脏停跳60 min时再灌注K-H液30 min。Sev组灌注液为饱含1 MAC七氟醚的K-H液,其余同IR组。观察并记录再灌注期间心律失常发生情况、心脏复跳时间和心律失常持续时间;记录平衡灌注15 min(T0)、继续灌注15 min/平衡30 min(T1)、再灌注15 min/平衡105 min(T2)、再灌注30 min/平衡120 min(T3)的左心室前壁外膜层和内膜层心肌单相动作电位(MAP),计算50%和90%单相动作电位时程(MAPD50、MAPD90);Western blot法和免疫组织化学法检测心肌组织Kir2.1蛋白相对含量和分布。结果灌注心脏复跳时IR组有6例发生心律失常,2 min内有1例恢复正常节律;Sev组有2例发生心律失常,2 min内有均恢复正常节律;IR组心脏复跳时间、心律失常持续时间明显长于Sev组(P<0.05);与T0和T1时比较,T2-T3时IR组外膜层和内膜层MAPD90明显延长(P<0.05);Sev组外膜层MAPD90明显延长(P<0.05)。T2-T3时Sev组和IR组外膜层和内膜层MAPD90明显长于C组(P<0.05),Sev组内膜层和外膜层MAPD90明显短于IR组(P<0.05)。IR组Kir2.1蛋白相对含量明显低于C组(P<0.05),Sev组Kir2.1蛋白相对含量明显高于IR组(P<0.05);C组Kir2.1蛋白呈强阳性表达,且具有规则的分布;IR组Kir2.1蛋白的表达点状分散分布且无规律;Sev组Kir2.1蛋白呈强阳性表达,且具有规则的分布。结论七氟醚降低低温全心缺血-再灌注心律失常的发生,其分子机制可能与Kir2.1蛋白的表达与�Objective To observe the effect of sevoflurane on the expression of Kir2.1 protein in myocardial tissue of arrhythmia induced by hypothermic global ischemia-reperfusion.Methods Twenty-four healthy adult male SD rats,weighing 280-320 g,were successfully prepared into Langendorff isolated heart perfusion model.After 15 min of K-H liquid equilibrium perfusion,they were randomly divided into three groups(n=8):control group(group C),hypothermic global ischemia-reperfusion group(group IR)and sevoflurane group(group Sev).In group C,K-H fluid was continuously perfused for 105 min.In group IR,after 15 min of continuous perfusion of K-H solution,Thomas solution(4℃,20 ml/kg)was injected to make the heart stop beating.When the heart stopped beating for 30 minutes,Thomas solution(4℃,10 ml/kg)was added.When the heart stopped beating for 60 min,K-H solution was reperfused for 30 min.In group Sev,K-H fluid contained 1.0 MAC sevoflurane and other procedures were the same as that in group IR.The occurence of arrhythmia were recorded during the period of reperfusion.MAP S including time course(MAPD 50 and MAPD 90)of endocardium and epicardium was recorded at the time of balanced perfusion for 15 min(T 0),continuous perfusion for 15 min(T 1),reperfusion for 15 min/continuous perfusion for 105 min(T 2)and reperfusion for 30 min/continuous perfusion for 120 min(T 3).The expression and distribution of Kir2.1 protein in myocardium were detected by immunoblotting and immunohistochemistry.Results Arrhythmias occurred in 6 cases in group IR and returned to normal rhythm in 1 case within 2 min,and that occurred in 2 cases in group Sev and returned to normal rhythm in 2 min.The development of arrhythmia and time for restoration of spontaneous heart beat in group IR were significantly longer than those in group Sev(P<0.05);Compared with T 0-T 1,MAPD 90 in the outer and inner membrane of group IR was significantly longer(P<0.05),and MAPD 90 in the outer membrane of group Sev was significantly longer(P<0.05).At T 2-T 3,MAPD 90 of outer and
关 键 词:七氟醚 低温全心缺血-再灌注 再灌注心律失常 Kir2.1蛋白
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