本文選題：右美托咪定 + 缺血-再灌注損傷　； 參考：《臨床麻醉學雜志》2017年04期

【摘要】：目的觀察右美托咪定對離體家兔心缺血-再灌注(ischemia-reperfusion,IR)損傷后心肌復極不均一性及Cx43表達的影響,探討Cx43在右美托咪定抑制IR損傷心肌復極不均一性中的作用。方法健康成年家兔18只,體重(2.0±0.5)kg,成功制備Langendorff離體心臟灌注模型,KH液平衡灌流15min后隨機均分為三組,每組6只�？瞻讓φ战M(C組):持續(xù)平衡灌注37℃K-H液150min;IR組:K-H液繼續(xù)灌流15 min后停灌,注射4℃Thomas液10 ml/kg使心臟停搏60min,心臟周圍用4℃Thomas液保護,30min半量復灌4℃Thomas液5ml/kg,60min時復灌K-H液;右美托咪定組(DEX組):于K-H液及Thomas液中加入右美托咪定25ng/ml,余同IR組。記錄平衡灌流15min(T_0)、繼續(xù)灌流15min(平衡30min,T_1)、復灌30min(平衡120min,T_2)、復灌60min(平衡150min,T_3)的HR及三層心肌(內(nèi)膜、中膜、外膜)90%單相動作電位時程(MAPD90)并以此計算跨室壁復極離散度(transmural dispersion of repolarization,TDR),觀察心臟復灌時心律失常發(fā)生情況、復跳時間,T_3時取左心室組織采用Western blot法、免疫組化法檢測左室心肌組織Cx43的表達及分布。結(jié)果 DEX組復跳時間明顯短于IR組(P0.05);與T_0時比較,T_2、T_3時IR組、DEX組HR明顯減慢,TDR明顯增大(P0.05);與IR組比較,T_1~T_3時DEX組HR明顯減慢,T_2、T_3時DEX組TDR明顯減小(P0.05)。與C組比較,IR組、DEX組Cx43表達明顯減少(P0.05)且分布不均,且DEX組明顯多于IR組(P0.05)。結(jié)論右美托咪定抑制IR損傷后心肌復極不均一性,從而起到穩(wěn)定IR損傷心肌心電傳導,降低復灌性心律失常發(fā)生率的作用,其機制可能與右美托咪定抑制縫隙連接失偶聯(lián)、抑制Cx43表達減少及分布紊亂有關(guān)。
[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 鹵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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