右美托咪定对离体兔心室肌单相动作电位的影响  

Effect of dexmedetomidine on ventricular monophasic action potentials in isolated heart of rabbit

作　　者：龙娟[1] 高鸿[1,2] 刘艳秋[1,2] 丁华[3] 李惠[1] 张凯强[1] 钟毅[1,2] 

机构地区：[1]贵州医科大学麻醉学院,贵阳市550004 [2]贵州医科大学附属医院麻醉科,贵阳市550004 [3]贵州省人民医院泌尿外科,贵阳市550004

出　　处：《广西医学》2016年第8期1058-1061,1071,共5页Guangxi Medical Journal

基　　金：贵州省科技厅自然科学基金(黔科合LG字[2011]015号)

摘　　要：目的 探讨右美托咪定对离体兔心室肌单相动作电位的影响。方法 成年新西兰大白兔18只，制备Langendorff离体心脏灌注模型，Krebs-Hensleit（K-H）液平衡灌注15 min后随机分为3组各6只。正常对照组（C组）继续灌注37℃ K-H液60 min；低浓度右美托咪定组（L组）灌注含25 ng/ml右美托咪定的K-H液60 min；高浓度右美托咪定组（H组）灌注含50 ng/ml右美托咪定的K-H液60 min。记录平衡灌注15 min（T0）、继续灌注15 min（T1）、30 min（T2）、60 min（T3）时左心室前壁3层心肌单相动作电位振幅、0期最大去极化速率（Vmax），计算单相动作电位复极50%和90%的时程（MAPD50和MAPD90），记录早期后除极、延迟后除极及心律失常的发生情况。结果 心肌在不同时间点的MAPA及Vmax的比较，差异无统计学意义（P＞0.05）。在T1～T3，H组的MAPD50及MAPD90较C组和L组延长（P＜0.05）；与T0比较，T1～T3时H组MAPD50、MAPD90明显延长（P＜0.05）；在各个时间点，L组与C组的MAPD50和MAPD90差异均无统计学意义（P＞0.05）。结论 高浓度右美托咪定可以延长MAPD50和MAPD90，这可能是其增加心律失常发生风险的机制。Objective To explore the effect of dexmedetomidine on monophasic action potentials （MAP） of myocardium in isolated hearts of rabbit. Methods Langendorff isolated heart perfusion model was established in 18 adult New Zealand rabbits. The models were randomly divided into three groups after 15 minutes of perfusion with Krebs-Hensleit（K-H） solution with 6 hearts in each group. The normal control group （Group C） continued to be perfused with 37℃ K-H solution for 60 minutes. Low-concentration dexmedetomidine group （Group L） was perfused with K-H solution containing 25 ng/ml dexmedetomidine for 60 minutes. High-concentration dexmedetomidine group （Group H） was perfused with K-H solution containing 50 ng/ml K-H dexmedetomidine for 60 minutes. Monophasic action potential amplitude （MAPA） and maximal velocity of 0 phase（Vmax） of three myocardial layers in left ventricular anterior wall were recorded at 15 minutes after perfusion（T0） ,at 15（T1） ,30（T2） and 60 minutes（T3） after additional perfusion. Then 50% and 90% of monophasie action potential duration（ MAPD50/MAPD90 ） were calculated. The incidences of early afterdepolarizations, delayed afterdepolarization and arrhythmia were also recorded. Results There were no statistical differences in myocardial MAPA or Vmax among different time points （P 〉 0.05 ）. At T1 ,T2 and T3, MAPD50 and MAPD90 of Group H were longer than those of Group C or Group L（P 〈 0.05 ）. In Group H, MAPDs0 and MAPDgo at T1, T2 and T3 were significantly longer than those at To （ P 〈 0.05 ）. At each time point, there were no statistical differences in MAPD50 or MAPD90 between Group L and Group C （P 〉 0.05 ）. Conclusion Dexmedetomidine with higher concentration can prolong MAPD50 and MAPD50 ,which may be the mechanism of increased arrhythmias risk caused by dexmedetomidine.

关 键 词：右美托咪定 单相动作电位 离体心脏 免 心室肌 

分 类 号：R614.2[医药卫生—麻醉学]