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作 者:安丽[1] 高鸿[1] 段宏伟 张凯强[3] 刘艳秋[1] 龙娟[3] 李惠[3] 钟毅[1]
机构地区:[1]贵州医科大学附属医院麻醉科,贵阳市550004 [2]上海市浦东医院麻醉科,上海市201399 [3]贵州医科大学麻醉学系,贵阳市550004
出 处:《实用医学杂志》2015年第21期3496-3498,共3页The Journal of Practical Medicine
基 金:贵州省卫生计生委科学技术基金项目(编号:gzwjkj2014-1-033)
摘 要:目的:探讨右美托咪定致心动过缓的心脏电生理机制及其与钾通道的关系。方法:成年家兔18只,体重2.0-2.5 kg,制备Langendorff离体心脏模型,K-H液平衡灌注15 min后随机分为3组(n=6):对照组(C组)继续灌注K-H液60 min;右美托咪定组(D组)灌注含0.05μg/L右美托咪定的K-H液60 min;四乙胺组(K组)灌注含10 mmol/L四乙胺的K-H液60 min。记录平衡灌注15 min(T0)、继续灌注15、30、60 min(T1-T3)时HR、单相动作电位(MAP),计算动作电位复极50%、90%的时程(MAPD50、MAPD90)。记录心律失常的发生情况。结果:与T0比较,D组和K组T1-T3时HR减慢(P〈0.01),MAPD50、MAPD90延长(P〈0.05);与C组比较,D组和K组HR减慢(P〈0.01),MAPD50、MAPD90延长(P〈0.05)。结论:右美托咪定可能通过阻滞心肌细胞膜钾离子通道,引起动作电位时程延长,从而导致心率减慢。Objective To investigate the mechanism of dexmedetomidine-induced bradycardia on cardiac electrophysiology and its relationship with potassium channels. Methods Isolated heart perfusion models from eighteen adult rabbits, weighing 2.0 - 2.5 kg, were prepared by Langendorff and the hearts were randomly di- vided into three groups after peffusion with K-H 15 minutes (n = 6): control group (group C, continuous perfusion 60 min), dexmedetomidine group (group D, perfusion with 0.05 μg/L of dexmedetomidine K-H solution 60 min) and voltage-gated potassium channel blocker tetraethyla mmonium group (group K, perfusion fluid containing 10 mmol/L K-H tetraethyla mmonium). HR, three layer myocardial monophasie action potential (MAP) of left ventrieular anterior wall after balanced infusion 15 min (T0), continued perfusion 15, 30, 60 min (T1 - T3) were recorded. The monophasic action potential duration of repolarization at 90% and 50% were calculated respectively. The occurrence of arrhythmia were also observed. Results In group D and group K, there were slower HR (P 〈 0.01) and longer MAPD50 and MAPD90 at T1 - T3 than those at T0 (P 〈 0.05) and in Group D and group K, there were slower HR (P 〈 0.01 ) and longer MAPD50 and MAPD90 than those in group C (P 〈 0.05 ). Conclusion Dexmedetomidine may block function of potassium channels on myocardial cell membrane, which causes the prolonging of monophasic action potential duration, resulting in slow heart beat.
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