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机构地区:[1]第三军医大学新桥医院麻醉科,重庆400037
出 处:《中国药理学通报》2010年第11期1501-1504,共4页Chinese Pharmacological Bulletin
摘 要:目的观察阿米替林(Amitriptyline,AMI)对分支选择结扎模型(spared nerve injury,SNI)大鼠脑脊液(Cerebrospi-nal Fluid,CSF)中EAAs-IAAs的影响。方法 30只♂SD大鼠,随机分为对照组(A组)、SNI模型组(B组)、SNI+AMI组(C组),A组和B组经腹腔注射分别给予0.2ml生理盐水、C组腹腔注射给予10mg·kg-1阿米替林,每日2次。在动物模型制做前0d及后1、3、5d测量各组大鼠机械痛阈并在体测量CSF中谷氨酸(Glu)、天冬氨酸(Asp)、γ-氨基丁酸(GABA)、甘氨酸(Gly)。结果与A组相比,B组大鼠机械痛阈值随时间下降明显(P<0.01),Glu、Asp的表达随时间推移逐渐增加(P<0.01),GABA、Gly的表达在术后1d升高(P<0.01和P<0.05),在术后3d下降(P<0.01和P<0.05)、术后5d下降(P<0.01);C组大鼠较B组机械痛阈值提高(P<0.01),Glu、Asp的表达在术后3、5d下降(P<0.01),GABA、Gly的表达在术后5d升高(P<0.01)。结论 AMI可能通过纠正脊髓水平EAAs-IAAs失衡,减轻外周损害,治疗神经病理性疼痛。Aim To investigate the effect amitriptyline on EAAs-IAAs in spinal cord CSF of rats with spared nerve injury (SNI).Methods A total of 30 male SD rats were randomly divided into 3 groups with 10 rats in each group:control (A),SNI (B) and SNI+ amitriptyline (C) groups,which respectively were treated with intraperitoneal injections of 0.2 ml normal saline (A and B),10mg·kg-1 amitriptyline (C),bid.Mechanical pain threshold change of each group was measured and in vivo CSF Glu,Asp,GABA and Gly concentration were measured at the 0 day,1st day,3rd day,and 5th day after model was made.Results Compared with control,group B had a markedly decreased rat mechanical pain threshold (P0.01) and an obviously high expression of Glu and Asp levels at the corresponding time points(P0.01).GABA and Gly expression were increased in 1st day after surgery(P0.01and P0.05) and decreased in 3th day after surgery(P0.01 and P0.05) and decreased in 5th day after surgery(P0.01).And group C,compared with group B,mechanical pain threshold was markedly increased(P0.01).Not only Glu and Asp expression were significantly decreased in 3rd and 5th day after surgery(P0.01),but also GABA and Gly expression had a marked increase in 5th day after surgery(P0.01).Conclusion This result provides a new line of evidence that amitriptyline can restore of EAAs-IAAs balance at the spinal level to prevent peripheral injury,which may be one of its mechanisms in the treatment of neuropathic pain.
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