【摘要】 目的观察右美托咪定对家兔离体缺血—再灌注心脏心肌单相动作电位及突触素表达的影响,探讨其对缺血—再灌注心肌心电传导的影响。方法健康成年家兔,体质量（2.0±0.5）kg,成功制备Langendorff离体心脏灌注模型18例,K-H液平衡灌流15 min后,随机均分为三组（n=6）:空白对照组（C组）:持续平衡灌注37℃K-H液150 min;缺血—再灌注组（IR组）:K-H液继续灌流15 min后停灌,注射Thomas液（4℃,10 mL/kg）使心脏停搏60 min,心脏周围用低温（4℃）Thomas液保护,30 min半量复灌Thomas液（4℃,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（T₂）/平衡120 min、复灌60 min/平衡150 min（T₃）的HR及三层心肌（内膜（Endo）、中膜（Mid）、外膜（Epi））90%单相动作电位时程(monophonic action potential duration,MAPD₉₀),观察心脏复灌时心律失常、复跳时间并记录T₂时点三组3层心肌MAP图,免疫组化法检测心肌组织突触素（Synaptophysin,SYN）的表达,三组均不使用药物恢复心律。结果 DEX组心脏复跳时间明显短于IR组（P<0.05）;心脏复跳时IR组有6例发生心律失常,2 min内有2例恢复正常节律;DEX组有2例发生心律失常,2 min内有1例恢复正常节律;与T₀时比较,IR组T₂、T₃时HR明显减慢（P<0.05）,DEX组T₁～T₃时HR明显减慢,MAPD₉₀明显增大（P<0.05）;与C组比较,T₁～T₃时DEX组HR明显减慢,MAPD₉₀明显增大（P<0.05）;与IR组比较,T₁～T₃时DEX组HR明显减慢,MAPD₉₀明显增大（P<0.05）;SYN表达情况:IR组较C组明显减少（P<0.05）,DEX组较IR组表达增多但不及C组（P<0.05）。结论右美托咪定延长MAPD、抑制缺血—再灌注损伤后心肌突触素表达的减少,具有稳定缺血—再灌注心肌心电传导的作用。更多还原

【Abstract】 Objective To observe the effects of dexmedetomidine on the Monophasic Action Poten and expression of synaptophysin on ischemia reperfusion of isolated rabbit hearts, and investigate the effect of ischemia reperfusion myocardium on cardiac electrical conduction. Methods The healthy adult rabbits（2.0±0.5） kg, were randomly divided into 3 groups after Langendorff isolated heart perfusion model has been prepared in 18 cases and K-H fluid has 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 the ischemia/reperfusion group（group I/R）, 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 low temperature Thomas solution（4 ℃） around. Following the reperfusion of Thomas solution（4 ℃,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 given group（group DEX）. Dexmedetomidine was added in the K-H fluid and the Thomas solution（25 ng/mL）. The other procedures were the same as the I/R group. The heart rate（HR）, 90% monophasic action potential duration（MAPD90） of the three layers of myocardial（endometrium, membrane and epicardial）, 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 60 min/balance 150 min（T₃）. The arrhythmia and the resuscitation time at cardiac reperfusion were observed,and The MAP map of three groups of three layers of was recorded at T₂ time point. And was detected expression of synaptophysin（Synaptophysin, SYN） of myocardial tissue by immunohistochemical method. Not using drugs to restore heart rhythm. Results Group DEX cardiac resuscitation time was significantly shorter than group IR（P<0.05）. At the recovery of heart beating, group IR, six cases of arrhythmia, there were two cases within 2 min restore normal arrhythmia. Group DEX, twocases arrhythmia, one case within 2 min restore normal rhythm, no use of drugs to restore arrhythmia. Compared with T0 point, group I/R T₂,T₃ point HR lower（P<0.05）, group DEX T₁～T₃ point HR lower and MAPD90 increased（P<0.05）. Compared with group C, T₁～T₃ point group DEX HR lower and MAPD90 increased（P<0.05）. Compared with the group IR, at T₁～T₃ point lower group DEX HR and MAPD90 increased（P<0.05）. SYN expression: IR group than the C group was significantly reduced（P<0.05）, DEX group than the IR group was increased, but less than C group（P<0.05）. Conclusion Dexmedetomidine can prolong MAPD and inhibit the reduced expression of synaptophysin of ischemia reperfusion myocardial injury. There are effects of stable ischemia-reperfusion myocardium on cardiac electrical conduction.更多还原