文章摘要
王志华 邹丽丽 张巧梅 吴畏 李健楠 张丽娜 孟尽海.Orexin-A介导histamine能神经系统促进氯胺酮麻醉觉醒[J].,2015,15(14):2663-2665
Orexin-A介导histamine能神经系统促进氯胺酮麻醉觉醒
Orexin-A Facilitates Emergence fromKatemine Anesthesia throughHistaminergic System
  
DOI:
中文关键词: orexin-A  orexin-B  诱导时间  觉醒时间
英文关键词: Orexin-A  Orexin-B  LORR  RORR
基金项目:国家自然科学基金青年基金项目(81401138);宁夏医科大学科学研究基金面上项目(XM201321)
作者单位
王志华 邹丽丽 张巧梅 吴畏 李健楠 张丽娜 孟尽海 宁夏医科大学总医院麻醉科第四军医大学西京医院麻醉科 
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中文摘要:
      目的:探索氯胺酮麻醉下,Orexin 神经信号是否激活结节乳头体核(Tuberomammillary Nucleus,TMN)促进大鼠氯胺酮麻 醉觉醒。方法:成年雄性SD 大鼠(体重230-280 g),在10%水合氯醛麻醉下(1 ml/kg,i.p.)进行以下实验:①TMN 核团埋置微注射 外套管,回笼单独饲养7 天后,大鼠随机分为三组,分别为对照组(NS)、orexin-A 组与orexin-B组。TMN 核团分别双侧微注射NS (0.3 滋L)、orexin-A(100 pmol/0.3 滋L)及orexin-B(100 pmol/0.3 滋L)观察氯胺酮麻醉下(100 mg/kg, 腹腔注射)大鼠诱导时间与觉醒 时间;②上述实验7 天后,大鼠随机分为三组,分别为溶剂DMSO 组、SB334867 组与TCS-OX2-29 组,TMN 核团分别双侧微注射 DMSO(0.3 滋L)、orexin 1 型受体(the orexin type 1 receptor,OX1R)的拮抗剂SB334867(20 滋g/0.3 滋L)和orexin 2型受体(the orexin type 2 receptor,OX2R)的拮抗剂TCS-OX2-29(20 滋g/0.3 滋L)观察氯胺酮麻醉下大鼠诱导时间与觉醒时间。结果:①各组大 鼠的诱导时间无统计学差异。②在TMN 核团微注射orexin-A 与对照组相比明显缩短了大鼠的觉醒时间(43.17± 6.31 min vs 51.17± 4.45 min,P<0.05),而微注射orexin-B 与对照组相比并没有明显影响大鼠的觉醒时间(50.33± 3.50 min vs 51.17± 4.45 min,P>0.05)。③TMN 核团微注射OX1R 拮抗剂SB334867 较溶剂DMSO 组延长了麻醉觉醒时间(60.83± 8.84 min vs 49.00± 5.73 min,P<0.05),OX2R拮抗剂TCS-OX2-29 与溶剂DMSO组相比并没有明显影响大鼠的觉醒时间(50.83± 4.79 min vs 49.00± 5.73 min,P>0.05)。结论:本研究实验证据证实在氯胺酮麻醉下,orexin 神经信号可能通过激活TMN 区组胺能神经系统促进麻醉 向觉醒的转换。
英文摘要:
      Objective:The aim of this study was to test whether activation of orexin signal in Tuberomammillary Nucleus (TMN) can facilitate emergence from katemine anesthesia or not.Methods:Adult male SD rats (body weight 230-280 g) were anesthetized by10% chloral hydrate (1 ml/kg, ip) to do the following work. ① Guide cannulas for microinjection to the TMN were embedded. Then the rats were fed in separate cage. Seven days later, rats were randomly divided into three groups. And then orexin-A (100 pmol/0.3 uL) , orexin-B (100 pmol/0.3 uL) and and their solvent NS (0.3 uL) were microinjected into TMN respectively to observe the induction time and awakening time in rats. ② The same operation as step 1, Seven days later, rats were grouped randomly. And then the OX1R antagonist SB334867 (20 uL/0.3 uL), OX2R antagonist TCS-OX2-29 and their solvent DMSO (0.3 uL) were microinjected into TMN respectively to observe the time of induction and awakening in rats.Results:① No statistical difference of induction time was found in each group. ②The rats which injected orexin-A (100 pmol/0.3 uL) recovered much faster from ketamine anesthesia (100 mg/kg, ip) than controlled group (injected NS 0.3 uL) (43.17± 6.31 min vs 51.17± 4.45 min,P<0.05).There was no significant difference on the emergence from ketamine anesthesia between the rats received orexin-B and controlled rats (50.33± 3.50 min vs 51.17± 4.45 min, P>0.05). ③ The injection of OX1R antagonist SB334867 (20 uL/0.3 uL) to TMN could prolong the emergence time from ketamine anesthesia compared to the solvent DMSO (0.3 uL) group (60.83± 8.84 min vs 49.00± 5.73 min, P<0.05). The injection of OX2R antagonist TCS-OX2-29 did not significantly affect the rat emergence time (50.83± 4.79 min vs 49.00± 5.73 min, P>0.05).Conclusion:Orexin-A Can facilitates emergence awakening fromketamine anesthesia through histaminergic systemin TMN.
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