缝隙连接Cx43在右美托咪定预防缺血-再灌注离体兔心复灌性心律失常中的作用

发布时间：2018-06-17 00:00

  本文选题：右美托咪定 + 缺血-再灌注损伤　； 参考：《临床麻醉学杂志》2017年04期

【摘要】：目的观察右美托咪定对离体家兔心缺血-再灌注(ischemia-reperfusion,IR)损伤后心肌复极不均一性及Cx43表达的影响,探讨Cx43在右美托咪定抑制IR损伤心肌复极不均一性中的作用。方法健康成年家兔18只,体重(2.0±0.5)kg,成功制备Langendorff离体心脏灌注模型,KH液平衡灌流15min后随机均分为三组,每组6只。空白对照组(C组):持续平衡灌注37℃K-H液150min;IR组:K-H液继续灌流15 min后停灌,注射4℃Thomas液10 ml/kg使心脏停搏60min,心脏周围用4℃Thomas液保护,30min半量复灌4℃Thomas液5ml/kg,60min时复灌K-H液;右美托咪定组(DEX组):于K-H液及Thomas液中加入右美托咪定25ng/ml,余同IR组。记录平衡灌流15min(T_0)、继续灌流15min(平衡30min,T_1)、复灌30min(平衡120min,T_2)、复灌60min(平衡150min,T_3)的HR及三层心肌(内膜、中膜、外膜)90%单相动作电位时程(MAPD90)并以此计算跨室壁复极离散度(transmural dispersion of repolarization,TDR),观察心脏复灌时心律失常发生情况、复跳时间,T_3时取左心室组织采用Western blot法、免疫组化法检测左室心肌组织Cx43的表达及分布。结果 DEX组复跳时间明显短于IR组(P0.05);与T_0时比较,T_2、T_3时IR组、DEX组HR明显减慢,TDR明显增大(P0.05);与IR组比较,T_1~T_3时DEX组HR明显减慢,T_2、T_3时DEX组TDR明显减小(P0.05)。与C组比较,IR组、DEX组Cx43表达明显减少(P0.05)且分布不均,且DEX组明显多于IR组(P0.05)。结论右美托咪定抑制IR损伤后心肌复极不均一性,从而起到稳定IR损伤心肌心电传导,降低复灌性心律失常发生率的作用,其机制可能与右美托咪定抑制缝隙连接失偶联、抑制Cx43表达减少及分布紊乱有关。
[Abstract]:Objective to observe the effects of dexmetomidine on myocardial repolarization heterogeneity and Cx43 expression after ischemia reperfusion (IRI) injury in isolated rabbit hearts, and to explore the role of dexmetomidine in inhibiting myocardial repolarization heterogeneity in IR injury. Methods 18 healthy adult rabbits were randomly divided into three groups (n = 6 in each group). Langendorff model of isolated heart perfusion was successfully prepared by equilibrium perfusion of KH solution with 15min in 2. 0 卤0. 5 渭 g 路kg 路L ~ (-1) 路L ~ (-1) 路L ~ (-1) 路L ~ (-1). Control group C: continuous equilibrium perfusion of 37 鈩，

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