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| ZP123可预防右美托咪定延长心肌复极时程所致的负性变频效应 |
| Efficacy of rotigaptide on prevention of negative chronotropic effect caused by dexmedetomidine lengthening myocardial repolarization duration |
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| DOI： |
| 中文关键词: 缝隙连接改造剂 右美托咪定 单相动作电位 |
| 英文关键词: Rotigaptide Dexmedetomidine Monophasic action potentials |
| 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 探讨缝隙连接改造剂ZP123对右美托咪定诱发鼠离体心脏复极时程延长所致的负性变频效应。方法 健康成年SD大鼠18只,雌雄不拘,体重(300±30)g,制备Langendorff离体心脏灌注模型,K-H液平衡灌注15 min后,随机分为三组,每组6只:空白对照组(C组)继续灌注37℃ K-H液30 min;右美托咪定组(D组)灌注含50 ng／ml右美托咪定的K-H液30 min,右美托咪定+ZP123组(ZD组)灌注含50 ng／ml右美托咪定+80 nmol／L ZP123的K-H液30 min。于平衡灌注15 min(To)、继续灌注15 min(T1)、30 min(T2)时记录HR和左心室心肌单相动作电位(MAP),计算MAP复极50％、90％的时程(MAPD50、MAPD90)、单相动电位振幅(MAPA)和最大去极化速度(Vmax)。结果 与T0 时比较,T1、T2时D组HR明显减慢(P<0.05),T1、T2时D组HR明显慢于C组和ZD组(P<0.05)。与T0 时比较,T1、T2时D组心肌MAPD50、MAPD90明显延长（P<0.05）;T1、T2时D组心肌MAPD50、MAPD90明显长于C组和ZD组(P<0.05)。三组心肌内外两层膜MAPA和Vmax组间组内差异均无统计学意义。结论 缝隙连接改造剂ZP123通过缩短心肌单相动作电位复极的时程从而拮抗右美托咪定诱发的鼠离体心脏的负性变频效应。 |
| 英文摘要: |
| Objective To evaluate efficacy of rotigaptide ZP123 on prevention of negative chronotropic effect caused by dexmedetomidine lengthening repolarization duration of the isolated rat hearts. Methods Eighteen healthy adult SD rats of either gender, weighing (300±30) g, were prepared isolated heart perfusion model by Langendorff. After 15 min perfusion and balance of K-H fluid, the isolated hearts were randomly divided into 3 groups (n=6 each): The hearts were continuously pefused for 30 min with 37℃ K-H solution in control group (group C), with dexmedetomidine 50 ng／ml in dexmedetomidine group (group D), or with rotigaptide 80 nmol／L combined with dexmedetomidine 50 ng／ml in rotigaptide combined with dexmedetomidine group (group ZD). In the whole Langendorff-perfused hearts, at the end of balanced infusion for 15 min (T0 ) and at 15(T1), 30(T2) min of continued perfusion with K-H solution, the monophasic action potential (MAP) and heart rate (HR) were recorded from left anterior free wall, MAP duration at 50％ repolarization (MAPD50) and at 90％ repolarization (MAPD90), monophasic action potential amplitude (MAPA) and maximal velocity (Vmax) were calculated. Results Compared with T0 , HR in group D was significantly declined at T1, T2; MAPD90 and MAPD50 in group D were significantly increased at T1, T2 (P<0.05). Compared with groups C and ZD, HR in group D was significantly declined at T1, T2; MAPD90 and MAPD50 in group D were significantly increased at T1, T2 (P<0.05). There was no significant difference in MAPA and Vmax between the three groups． Conclusion Rotigaptide antagonizes negative chronotropic effect induced by dexmedetomidine through shortening monophasic action potential duration in the myocardium of left ventricle of the isolated rat hearts. |
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