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| 不同浓度七氟醚对缺血-再灌注心肌单相动作电位影响 |
| Effects of different concentrations of sevoflurane on monophasic action potential of myocardium of ischemia-reperfusion |
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| DOI：10.12089/jca.2018.05.015 |
| 中文关键词: 七氟醚 离体心脏 缺血-再灌注 单相动作电位 |
| 英文关键词: Sevoflurane Isolated heart Ischemia-reperfusion Monophasic action potential |
| 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 观察不同浓度七氟醚对大鼠离体心脏缺血-再灌注时心肌单相动作电位（MAP）的影响。方法 健康成年雄性SD大鼠32只, 体重280～320 g, 成功制备langendorff离体心脏灌注模型, K-H液平衡灌注15 min后, 随机分为四组, 每组8只: 缺血-再灌注组(IR组): K-H液继续灌注15 min后停止, 注射Thomas液(4℃, 20 ml/kg)使心脏停搏60 min, 心脏周围用低温(4℃)Thomas液保护, 30 min时半量复灌Thomas液(4℃, 10 ml/kg), 60 min时再灌注K-H液30 min;0.5 MAC七氟醚组(Sev0.5组): K-H液为含饱和0.5 MAC七氟醚液体, 余同IR组;1.0 MAC七氟醚组(Sev1.0组): K-H液为含饱和1.0 MAC七氟醚液体, 余同IR组;2.0 MAC七氟醚组(Sev2.0组): K-H液为含饱和2.0 MAC七氟醚液体, 余同IR组。记录平衡灌注15 min(T0)、继续灌注15 min(T1)、再灌注15 min(T2)、再灌注30 min(T3)的HR及左心室前壁外膜层、中层和内膜层心肌MAP, 计算MAP复极50％及90％的时程(MAPD50、MAPD90)。并记录心律失常发生情况。结果 与T0和T1时比较, T2、T3时IR组、Sev1.0组、Sev2.0组HR明显减慢(P＜0.05)；与IR组比较,T2、T3时Sev0.5组、Sev1.0组HR明显增快, Sev2.0组HR明显减慢(P＜0.05)。与IR组比较, T3时Sev0.5组MAPD50, Sev0.5组、Sev1.0组、Sev2.0组MAPD90明显缩短(P＜0.05)。心脏复跳时IR组有6例, Sev0.5组有1例, Sev1.0组有2例, Sev2.0组有1例发生心律失常，与IR组比较，Sev0.5组、Sev1.0组和Sev2.0组心律失常发生率明显降低(P＜0.05)。结论 不同浓度七氟醚均可缩短缺血-再灌注心肌单相动作电位MAPD90, 且这一作用在0.5～2.0 MAC的七氟醚浓度范围内无剂量依赖性,这可能是其减少缺血-再灌注心律失常发生风险的机制。 |
| 英文摘要: |
| Ojective To study the effects of different concentrations of sevoflurane on monophasic action potentials (MAPs) of three-layer myocardium of ischemia reperfusion in isolated rat hearts. Methods Thirty-two healthy SD male rats, weighing 280-320 g, were randomly divided into four groups after successful preparation of langendorff isolated heart perfusion model and 15 min perfusion and balance of K-H fluid. In the ischemia-reperfusion group(group IR), K-H fluid perfusion was stopped and balanced for 15 min and cardiac arrest was induced for 60 min with the injection of Thomas solution (4℃, 20 ml/kg) while the heart was protected by the low temperature Thomas solution (4℃) around it. Reperfusion of Thomas solution (4℃, 10 ml/kg) was performed for 30 min and the heart was resuscitated by the perfusion of K-H fluid for 60 min. In the 0.5 MAC sevoflurane group (group Sev0.5), K-H fluid contained 0.5 MAC sevoflurane and other procedures were the same as in group IR. 1.0 MAC sevoflurane group (group Sev1.0), K-H fluid contained 1.0 MAC sevoflurane and other procedures were the same as in group IR. 2.0 MAC sevoflurane group (group Sev2.0), K-H fluid contained 2.0 MAC sevoflurane and other procedures were same as in group IR. HR, MAPs including time course (MAPD50, MAPD90) and MAP amplitude of endocardium, mid-layer myodardium and epicardium was recorded at the time of continuous balance perfusion for 15 min (T0), continuous perfusion for 15 min (T1), reperfusion for 15 min (T2) and 30 min (T3). Results Compared with T0 and T1, HR was slower at T2 and T3 (P＜0.05); Compared with group IR at T2 and T3, HR in group Sev0.5 and group Sev1.0 was higher, that in group Sev2.0 was slower P＜0.05); At T2, arrhythmia was observed in 6 rats in group IR, while arrhythmia was observed in 1 rats in group Sev0.5, and arrhythmia was observed in 2 rats in group Sev1.0 and arrhythmia was observed in 1 rats in group Sev2.0;Compared with group IR at T3, MAPD50 in group Sev0.5 was shorter in three sites(P＜0.05); Compared with group IR at T3, MAPD90 in other three groups was shorter. Conclusion Different concentrations of sevoflurane can shorten MAPD90 of MAPs, and the effects dont depend on the concertrations of sevoflurane when it changes from 0.5 MAC to 2.0 MAC; which may be the mechanism of decreased arrhythmias risk caused by sevoflurane. |
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