文章摘要
不同温度下七氟醚对离体大鼠心肌电兴奋性及电传导功能的影响研究
Effects of sevoflurane on myocardial electrical excitability and electrical conduction function at different temperatures in isolated rat hearts
  
DOI：10.12089/jca.2019.05.020
中文关键词: 低温  七氟醚  传导速度  心肌电兴奋性  电传导功能
英文关键词: Hypothermia  Sevoflurane  Conduction velocity  Myocardial electrical excitability  Electrical conduction function
基金项目:贵州省科技厅联合基金(黔科合LH字[2016]7252号)；贵州省卫生计生委科学技术基金(gzwjkj2016-1-007)；贵州医科大学2017年高等学校大学生创新创业训练计划项目（201710660020）
作者单位E-mail
李华宇 550004,贵阳市,贵州医科大学麻醉学院  
高鸿 贵州医科大学附属医院麻醉科 2169617@qq.com 
刘艳秋 550004,贵阳市,贵州医科大学麻醉学院  
安丽 550004,贵阳市,贵州医科大学麻醉学院  
王贵龙 550004,贵阳市,贵州医科大学麻醉学院  
符校魁 550004,贵阳市,贵州医科大学麻醉学院  
代东君 550004,贵阳市,贵州医科大学麻醉学院  
王子君 550004,贵阳市,贵州医科大学麻醉学院  
李伟超 550004,贵阳市,贵州医科大学麻醉学院  
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中文摘要:
      
目的 观察在不同温度下七氟醚对离体大鼠心肌电兴奋性及电传导功能的影响。
方法 健康成年雄性SD大鼠36只,体重280～360 g，成功制备Langendorff离体心脏灌注模型,采用随机数字表法分为6组(n=6)。各组均用K-H液平衡灌注15 min后，正常对照组(C组)继续灌注37 ℃ K-H液30 min；35 ℃低温组（H1组）、32 ℃低温组（H2组）分别继续灌注35 ℃ K-H液及32 ℃ K-H液30 min；七氟醚组（S组）继续灌注含1.0 MAC七氟醚饱和的37 ℃ K-H液30 min；35 ℃低温联合七氟醚组(H1S组)和32 ℃低温联合七氟醚组(H2S组)分别继续灌注含1.0MAC七氟醚饱和的35 ℃K-H液及32 ℃K-H液30 min。于平衡灌注末、继续灌注30 min时记录HR。测量继续灌注30 min时有效不应期（ERP）及房室结2比1阻滞点（2∶1B)，并计算传导速度（CV）。记录心律失常的发生情况。
结果 与C组比较，H1组及H1S组继续灌注30 min时CV、ERP及2∶1B差异无统计学意义，H2组及H2S组继续灌注30 min时CV明显减慢、ERP明显延长及2：1B明显降低（P<0.05)；与S组比较，H2S组继续灌注30 min时CV明显减慢、ERP明显延长、2∶1B明显降低（P<0.05)；与H1组比较，H2组及H2S组继续灌注30 min时CV明显减慢、ERP明显延长、2∶1B明显降低（P<0.05)；与H2组比较，H2S组继续灌注30 min时CV明显增快、ERP明显缩短（P<0.05)，而2∶1B差异无统计学意义。H2S组室性心律失常的发生率明显低于H2组（P<0.05)。
结论 七氟醚可抑制低温引起的心肌电兴奋性降低并稳定电传导功能，从而降低低温诱发室性心律失常的风险。
英文摘要:
      
Ojective To observe the effects of sevoflurane on myocardial electrical excitability and electrical conduction function at different temperatures in isolated rat hearts.
Methods Healthy adult male SD rats, weighing 280 - 360 g were successfully prepared into 36 Langendorff isolated cardiac perfusion models, which were randomly divided into 6 groups (n=6) using a random number table. After each group was perfused with 37 ℃ K-H solution for 15 min, the control group (group C) continued to be perfused with 37 ℃ K-H solution for 30 mins; the 35 ℃ hypothermia group (group H1) and the 32 ℃ hypothermia group (group H2) continued to be perfused with 35 ℃ K-H solution and 32 ℃ K-H solution for 30 min respectivelly; the sevoflurane group (group S) continued to be perfused with 37 ℃ K-H solution containing 1.0 MAC sevoflurane saturation for 30 min; the 35 ℃ hypothermia combined with sevoflurane group (group H1S) and the 32 ℃ hypothermia combined with sevoflurane group (group H2S) countinued to perfuse with 1.0 MAC sevoflurane saturated 35 ℃ K-H solution and 32 ℃ K-H solution for 30 min respectivelly. The HR at the end of equilibrium perfusion and continued perfusion for 30 min was recorded. The effective refractory period (ERP), the atrioventricular node 2∶1 block (2∶1B) and calculating the conduction velocity (CV) were recorded after continued perfusion for 30 min. The occurrence of arrhythmia was recorded during the whole perfusion.
Results Compared with group C, there was no significant difference in CV, ERP and 2∶1B in group H1 and H1S after continued perfusion for 30 min; but in group H2 and H2S, CV was slowed down, ERP was prolonged and 2∶1B was decreased (P < 0.05); compared with group S, CV was slowed down, ERP was prolonged and 2∶1B was decreased after continued perfusion for 30 min in group H2S (P < 0.05); compared with group H1, CV was slowed down, ERP was prolonged and 2∶1B was decreased in groups H2 and H2S (P < 0.05); compared with group H2, CV was faster and ERP was shortened in group H2S ( P < 0.05), but there was no significant difference in 2∶1B. The incidence of ventricular arrhythmia was lower in group H2S than that in group H2 (P < 0.05).
Conclusion Sevoflurane can inhibit the decrease of myocardial electrical excitability and stabilize the electrical conduction function induced by hypothermia, thus reducing the risk of hypothermia-induced ventricular arrhythmia.
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