右美托咪定诱发大鼠窦性心动过缓时窦房结Cx45与Cx40表达的变化  

Changes in expression of Cx45 and Cx40 in sinoatrial node during dexmedetomidine-induced sinus bradycardia in rats

作　　者：路凯 祝瑜 钟毅 田磊 殷永强 高鸿 Lu Kai;Zhu Yu;Zhong Yi;Tian Lei;Yin Yongqiang;Gao Hong(Workstation for Graduate Students Majoring in Anesthesiology of Guizhou Province College of Anesthesiology,Guizhou Medical University,Guiyang 550004,China;Department of Anesthesiology,Affiliated Hospital of Guizhou Medical University,Guiyang 550004,China)

机构地区：[1]贵州省麻醉学专业学位研究生工作站贵州医科大学麻醉学院,贵阳550004 [2]贵州医科大学附属医院麻醉科,贵阳550004

出　　处：《中华麻醉学杂志》2019年第3期300-303,共4页Chinese Journal of Anesthesiology

基　　金：贵阳市科技计划项目(筑科合同20161001[50]号).

摘　　要：目的评价右美托咪定诱发大鼠窦性心动过缓时窦房结缝隙连接蛋白45(Cx45)与Cx40表达的变化.方法健康SD大鼠40只,体重250~300g,按随机数字表法分为5组(n=8):对照组(C组)静脉输注生理盐水;低剂量右美托咪定组(D1组)和高剂量右美托咪定组(D2组)分别静脉输注右美托咪定负荷剂量20和120μg∕kg,10min,随后分别以10、60μg·kg^-1·h^-1速率静脉输注110min;低剂量右美托咪定+阿托品组(D1A组)和高剂量右美托咪定组+阿托品组(D2A组)右美托咪定给药方法分别与D1组和D2组相同,右美托咪定负荷剂量结束时,静脉注射阿托品0.5mg.于右美托咪定给药前、右美托咪定给药10、60、120min时记录HR、MAP和SpO2,记录心动过缓发生情况;给药结束后取窦房结组织,分别采用Westernblot法和RT-PCR法测定Cx45和Cx40及其mRNA的表达水平.结果D1组和D2组心动过缓发生率100%;D1A组和D2A组使用阿托品后心动过缓发生率为0.与C组比较,其余4组HR和MAP降低,D1组和D2组Cx45及其mRNA表达上调,Cx40及其mRNA表达下调(P<0.05),D1A组和D2A组Cx45和Cx40及其mRNA表达差异无统计学意义(P>0.05);与D1组比较,D1A组HR和MAP升高,Cx45及其mRNA表达下调,Cx40及其mRNA表达上调(P<0.05);与D2组比较,D2A组HR和MAP升高,Cx45及其mRNA表达下调,Cx40及其mRNA表达上调(P<0.05).结论右美托咪定诱发大鼠窦性心动过缓的机制可能与窦房结Cx45表达上调,Cx40表达下调有关;自主神经活动参与了右美托咪定对Cx45及Cx40表达的调控.Objective To evaluate the changes in the expression of Cx45 and Cx40 in the sinoatrial node during dexmedetomidine-induced sinus bradycardia in rats.Methods Forty healthy Sprague-Dawley rats,weighing 250-300 g,were divided into 5 groups(n=8 each)using a random number table method:control group(group C),low-dose dexmedetomidine group(group D1),high-dose dexmedetomidine group(group D2),low-dose dexmedetomidine plus atropin group(group D1A),and high-dose dexmedetomidine plus atropin group(group D2A).Normal saline was intravenously infused in group C.Dexmedetomidine was intravenously infused for 10 min as a loading dose of 20 and 120μg/kg,followed by an infusion of 10 and 60μg·kg^-1·h^-1 for 110 min in D1 and D2 groups,respectively.In D1A and D2A groups,dexmedetomidine was correspondingly given according to the method previously described in D1 and D2 groups,and in addition atropin 0.5 mg was intravenously injected at the end of infusing the loading dose of dexmedetomidine.Heart rate(HR),mean arterial pressure(MAP)and SpO2 were recorded before giving dexmedetomidine and at 10,60 and 120 min after giving dexmedetomidine,and the development of bradycardia was recorded.The sinoatrial node tissues were obtained at the end of administration for determination of the expression of Cx45 and Cx40 protein and mRNA by Western blot and real-time polymerase chain reaction,respectively.Results The incidence of bradycardia was 100%in D1 and D2 groups and 0 after using atropin in D1A and D2A groups.Compared with group C,HR and MAP were significantly decreased in the other four groups,the expression of Cx45 protein and mRNA was up-regulated,and the expression of Cx40 protein and mRNA was down-regulated in D1 and D2 groups(P<0.05),and no significant change was found in the expression of Cx45 and Cx40 protein and mRNA in D1A and D2A groups(P>0.05).Compared with group D1,HR and MAP were significantly increased,the expression of Cx45 protein and mRNA was down-regulated,and the expression of Cx40 protein and mRNA was up-regulated in g

关 键 词：右美托咪啶 心动过缓 窦房结 连接蛋白类 

分 类 号：R614[医药卫生—麻醉学]