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| 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 |
| Role of gap junction Cx43 in dexmedetomidine for prevention of reperfusion induced arrhythmias during ischemia reperfusion in isolated rabbit hearts |
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| DOI： |
| 中文关键词: 右美托咪定 缺血 再灌注损伤 离体心脏 跨室壁复极离散度 缝隙连接 |
| 英文关键词: Dexmedetomidine Ischemia-reperfusion injury Isolated heart Transmural dispersion of repolarization Gap junction Cx43 |
| 基金项目:贵阳市科技计划项目（筑科合同[20151001]社31号） |
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| 中文摘要: |
| 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,K-H液平衡灌流15 min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150 min;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60 min,心脏周围用4℃ Thomas液保护,30 min半量复灌4℃ Thomas液5 ml/kg,60 min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25 ng/ml,余同IR组。记录平衡灌流15 min(T0)、继续灌流15 min(平衡30 min,T1)、复灌30 min(平衡120 min,T2)、复灌60 min(平衡150 min,T3)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,T3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(P＜0.05);与T0时比较,T2、T3时IR组、DEX组HR明显减慢，TDR明显增大(P＜0.05);与IR组比较，T1～T3时DEX组HR明显减慢，T2、T3时DEX组TDR明显减小(P＜0.05)。与C组比较,IR组、DEX组Cx43表达明显减少(P＜0.05)且分布不均,且DEX组明显多于IR组(P＜0.05)。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。 |
| 英文摘要: |
| Objective To investigate the effect of dexmedetomidine on myocardial repolarization heterogeneity and the expression of Cx43 during ischemia reperfusion and the role of Cx43 in the dexmedetomidine for inhibition of myocardial repolarization heterogeneity during ischemia reperfusion in isolated rabbit hearts. Methods Eighteen healthy adult rabbits, weighing (2.0±0.5) kg, were randomly divided into three groups after Langendorff isolated heart perfusion model had been prepared and K-H fluid had been perfused and balanced 15 min. In the control group (group C), 37℃ K-H fluid was continuously perfused and balanced for 150 min. In group IR, K-H fluid was stopped after perfusion continue filling for 15 min, and then made the cardiac stop for 60 min with the injection of Thomas solution 10 ml/kg while the heart was protected by the 4℃ Thomas solution around. Following the reperfusion of 4℃ Thomas solution 5 ml/kg was performed for 30 min and the heart was resuscitated by the perfusion of K-H fluid for 60 min. In dexmedetomidine group given (group DEX), dexmedetomidine was added in the K-H fluid and the Thomas solution 25 ng/ml. The other procedures were the same as those of group IR. The heart rate (HR), 90% monophasic action potential duration (MAPD90) were recorded at the time of balance perfusion record 15 min (T0), continue perfusion 15 min/balance 30 min (T1), reperfusion 30 min/balance 120 min (T2) and reperfusion 60min/balance 150 min (T3). The transmural dispersion of repolarization (TDR) was calculated. To observe the cardiac reperfusion arrhythmia and rebeating time and recording. Detection expression of Cx43 in the left ventricular myocardial by Western blot and immunohistochemistry at T3. Results Group DEX cardiac resuscitation time was significantly shorter than that of group IR (P＜0.05). In group DEX. Compared with T0, HR was significantly decreased and TDR was significantly increased in groups IR and DEX at T2, T3 (P＜0.05). Compared with group IR, the TDR of group DEX was significantly decreased at T2, T3 (P＜0.05). Compared with group C, the expression of Cx43 was decreased (P＜0.05) and the distribution was not uniform in groups IR and DEX. Compared with group IR, the expression of Cx43 was decreased (P＜0.05) and the distribution was improved in group DEX. Conclusion Dexmedetomidine could inhibits myocardial repolarization heterogeneity of ischemia reperfusion injury, and thus play a stable cardiac conduction, reduce reperfusion arrhythmias, and its mechanism may be that dexmedetomidine could inhibits gap junctional uncoupling and inhibits expression and distribution of connexins decreased. |
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