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纳洛酮对芬太尼引起的大鼠纹状体抗坏血酸 尿酸 多巴胺及其代谢产物释放的影响

The Effect of Naloxone on Fentanyl-Induced Changes in Striatal Ascorbic Acid Uric Acid Dopamine and its Metabolic Release in Rats
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摘要 目的探讨μ-受体在芬太尼引起的大鼠纹状体细胞外抗坏血酸(AA)、尿酸(UA)、多巴胺(DA)及其氧化代谢产物2,5二羟苯乙酸(DOPAC)+高香草酸(HVA)变化中的作用机制。方法应用脑微透析技术结合高效液相色谱-电化学法(HPLC-ECD)检测。结果腹腔注射芬太尼可引起大鼠纹状体DA,DOPAC+HVA,AA,UA释放明显增加,腹腔应用纳洛酮可明显抑制芬太尼引起大鼠纹状体DA,DOPAC+HVA,AA,UA释放的增加;而纹状体内应用纳洛酮不能够拮抗芬太尼引起大鼠纹状体DA,DOPAC+HVA,UA,AA释放增加。结论芬太尼增加大鼠纹状体细胞外AA、UA、DA及其氧化代谢产物的释放主要是通过纹状体外μ-受体而起作用。 Aim To investigate the mechanism of μ- receptor in fentanyl - induced changes in striatal extracellur AA, UA,DA and DOPAC ＋ HVA release. Methods Using microdialysis in combination with high performance liquid chromatography （HPLC） with electrochemical detection （ECD） to determinate the release of neurochemicals. Results Intraperitoneally fentanyl administration increases exeellular AA, DA, UA, DOPAC ＋ HVA concentrations significantly in the striatum of freely moving rats. Intraperitoneally naloxone administration could antagonize fentanyl - induced increase of AA, DA, DOPAC ＋ HVA and UA dialysate concentrations significantly; while naloxone, given intrastriatally, failed to affect these neurochemicals. Conclusion Fentanyl - induced AA, UA, DA, DOPAC ＋ HVA increased mainly through a μ-opioid receptor- mediated mechanism at extrastriatal sites.
作者 尚宇
机构地区 中国人民解放军第
出处 《解放军药学学报》 CAS 2005年第4期251-255,共5页 Pharmaceutical Journal of Chinese People's Liberation Army
关键词 芬太尼 纳洛酮 微透析 纹状体 μ-受体 Fentanyl Naloxone Microdialysis Striatmn μ-Receptor
分类号 R965 [医药卫生—药理学]
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参考文献14

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解放军药学学报
2005年 第4期

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