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NOS抑制剂L-NAME的镇痛、致痛和致瘫作用 被引量:9

NOS inhibitor L-NAME produces analgesia,hyperalgesia and paralysis in rats
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摘要 鞘内注射(it)NOS抑制剂L-NAME0.125~4μmol可剂量依赖性抑制大鼠足底注射Formalin引起的癌症反应,并有7/31大鼠出现迟发性一过性双后肢瘫痪。itLNAME5μmol对正常大鼠无明显影响,但10μmol和20μmol均引起明显的痛敏及截瘫.it另一NOS抑制剂氨基胍0.2~1.0μmol也显著抑制Formalin痛定反应,1.25~7.0μmol则引起正常大鼠剂量依赖性痛敏行为,但对后肢运动功能无影响。结果表明脊髓水平NO在痛觉传递与调制中起重要作用,过度抑制NO的产生可引起痛觉敏化和瘫痪。 Intrathecal administration(it) of NGNitro-L-Arginine Methyl Ester(L-NAME) 0.125 to 4μmol produced a dose-dependant inhibition of the formalin-induced nociceptive behavior(weighted score) in rats,some of which(7/31),however,showed a delayed transient hindlimb paralysis.In normal rats,it L-NAME 5μmol did not produce any behavioral abnormalities but higher dose of it LNAME(both 10μmol and 20μmol) induced significant paraplegia and hyperalgesia.Another nitric oxide synthase inhibitor,aminoguanidine,exhibited significant antinociception in the formalin test at dose of it 0.2 to 1μmol and produced a dose-dependant byperalgesia in normal rats at higher dose of 1.25 to 7umol but did not induce any motor dysfunction.These results suggested that nitric oxide plays a dual role in spinal nociceptive modulation and L-NAME produces spinal cord injury.
出处 《中国药理学通报》 CAS CSCD 北大核心 1996年第4期309-313,共5页 Chinese Pharmacological Bulletin
基金 国家自然科学基金
关键词 一氧化氮合成酶 L-NAME 脊髓 痛觉 神经损伤 nitric oxide synthase spinal cord pain rat injury
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