文章摘要
李顺洪,冯 麟,岳济民,李林佶,谢 颖.利多卡因对异氟醚麻醉后大鼠海马组织炎症及认知功能的影响[J].,2017,17(29):5633-5636
利多卡因对异氟醚麻醉后大鼠海马组织炎症及认知功能的影响
Effects of Lidocaine on Inflammation of Hippocampal Tissue and Cognitive Function after Isoflurane Anesthesia in Rats
投稿时间:2017-02-26  修订日期:2017-03-22
DOI:10.13241/j.cnki.pmb.2017.29.007
中文关键词: 利多卡因  异氟醚  炎症因子  神经活性物质
英文关键词: Lidocaine  Isoflurane  Inflammatory cytokines  Nerve active substance
基金项目:四川省教育厅科研重点项目(13ZA058);川北医学院博士科研启动基金项目(CBY13-QD-11)
作者单位E-mail
李顺洪 川北医学院第二临床学院、南充市中心医院麻醉科 四川 南充 637000 clj060402@yeah.net 
冯 麟 川北医学院第二临床学院、南充市中心医院麻醉科 四川 南充 637000  
岳济民 川北医学院第二临床学院、南充市中心医院麻醉科 四川 南充 637000  
李林佶 川北医学院第二临床学院、南充市中心医院麻醉科 四川 南充 637000  
谢 颖 川北医学院第二临床学院、南充市中心医院麻醉科 四川 南充 637000  
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中文摘要:
      摘要 目的:研究利多卡因对异氟醚麻醉后大鼠海马区炎症因子、神经活性物质及认知功能的影响。方法:60只老龄SD大鼠随机分为3组:异氟醚组、利多卡因+异氟醚组、对照组各20只,建立大鼠吸入麻醉模型。利多卡因+异氟醚组给予静脉注射利多卡因,其他组给予生理盐水作为对照。麻醉结束后24 h Morris水迷宫实验评价大鼠认知功能,ELISA法检测大鼠海马组织炎症因子和神经活性物质。结果:与对照组相比,异氟醚组Morris水迷宫逃避潜伏期延长(P<0.05),平台象限停留时间及穿越平台次数减少(P<0.05),海马组织TNF-α、IL-6、IL-1β水平升高(P<0.05),NT-3、NGF、BDNF水平降低(P<0.05)。利多卡因明显缩短异氟醚麻醉大鼠的逃避潜伏期并增加其平台象限停留时间及穿越平台次数(P<0.05),降低海马组织炎症水平(P<0.05),升高神经活性物质水平(P<0.05)。结论:利多卡因可明显缓解异氟醚麻醉后大鼠海马组织的炎症反应并升高海马组织神经活性物质水平,改善认知功能障碍。
英文摘要:
      ABSTRACT Objective: To investigate the effects of lidocaine on inflammatory cytokine, neural active substance and the cognitive impairments induced by isoflurane in aged mice. Methods: 60 aged SD mice were assigned randomly into 3 groups: isoflurane group, lidocaine+isoflurane group and control group. Inhalation anesthesia model was established in rats. The mice in lidocaine+isoflurane group were given intravenous lidocaine,and the mice in other groups were given intravenous normal saline as control. Morris water maze test was performed to examine cognitive function 24 h after isoflurane exposure, and the content of inflammatory cytokines and nerve active substance in rat hippocampal area were measured by ELISA. Results: Compared with the control group, the Morris water maze escape latency was prolonged(P<0.05), the residence time of the platform and the times of crossing platform were decreased(P<0.05), the levels of TNF-α, IL-6 and IL-1β were significantly increased in the hippocampus(P<0.05), the levels of NT-3, NGF and BDNF were decreased in the hippocampus in isoflurane group(P<0.05). Lidocaine can obviously shorten the escape latency(P<0.05), increase the residence time of the platform and the times of crossing platform(P<0.05), decrease levels of inflammatory cytokines(P<0.05), and increase levels of nerve active substance in rats hippocampus(P<0.05). Conclusion: Lidocaine can relieve inflammatory response and increased neural active substance in rats hippocampus after isoflurane anesthesia, and improve cognitive dysfunction.
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