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作 者:薛朝霞[1] 胡古月[2] 师瑾[1] 吕晓敏[1]
机构地区:[1]山西医科大学第一附属医院麻醉科,太原030001 [2]内蒙古赤峰市医院麻醉科,赤峰024000
出 处:《中国疼痛医学杂志》2013年第12期739-742,共4页Chinese Journal of Pain Medicine
摘 要:目的:探讨脊髓Gs蛋白在瑞芬太尼诱发切口痛大鼠痛觉过敏中的作用。方法:雄性SD大鼠采用数字表法随机分为6组(n=8),均做切口痛模型。对照组(I组)尾静脉泵注生理盐水;实验组(R组、C1组、C2组、U1组和U2组)均制备瑞芬太尼痛敏模型。R组:单纯泵注瑞芬太尼;C1、C2组分别静注小剂量和中剂量μ受体拮抗剂(CTOP)+瑞芬太尼;U1组:小剂量CTOP+κ受体激动剂(U-50488)+瑞芬太尼;U2组:中剂量CTOP+U-50488+瑞芬太尼。测定各组大鼠给药前、后2 h热痛刺激潜伏时间(paw withdrawal latency,PWL)及给药后大鼠脊髓Gs蛋白mRNA水平。结果:(1)行为学结果:与给药后I组相比,R组PWL明显缩短。与R组相比,C1、C2、U1和U2组PWL均延长,其中以U1组最为显著。(2)Gs蛋白结果:R组Gs mRNA水平较其余各组均高,C1、C2、U1和U2组Gs mRNA无差异。结论:瑞芬太尼诱发大鼠痛觉过敏时脊髓Gs mRNA表达增加。给予μ受体拮抗剂可使Gs mRNA水平降低,对抗瑞芬太尼诱发的痛敏效应。联合κ受体激动剂可获得更为明显的抗痛敏(或镇痛)效应,小剂量μ受体拮抗剂和κ受体激动剂较中等剂量更为有效。Objective:To observe the involvement of spinal Gs protein in remifentanil-induced hyperalgesia in rats.Methods:Male SD rats were randomly divided into six groups (n =8),all groups established incisional pain model.The control group (Ⅰ) was treated with continuous pumped saline through rat tail vein.All of the experiment groups were given remifentanil to establish pain sensitivity model.The group R received remifentanil only.Groups C 1 and C2 were administrated with low-dose and middle-dose of μ receptor antagonist (CTOP) respectively.The group U1 received low-dose CTOP + κ receptor agonist (U-50488) + remifentanil.The group U2 received middle-dose CTOP + U-50488 + remifentanil.Before drug administration and 2 hours after drug administration,paw withdrawal latency (PWL) to thermal stimulation was measured on the right hindpaw (ipsilateral to incisional) in all groups.After behavior test,the expression level of Gs mRNA in the spinal cord was detected by RT-PCR.Results:(1) After drug administration,PWL of group R was significant shorter than that of group Ⅰ.Compared with group R,PWLs of groups C1,C2,U1 and U2 were increased significantly,particularly in groups U1.(2) The expression level of Gs mRNA in group R was higher than other groups and there were no statistically significance among groups C1,C2,U1 and U2.Conclusion:The expression of GS mRNA in rat spinal cord was increased in remifentanil-induced hyperalgesia rats.The μt receptor antagonist significantly decreased the Gs mRNA level and antagonized remifentanil-induced thermal hyperalgesia.Combination of μ receptor antagonist and κ receptor agonist produced more efficient analgesia.The analgesic effects of combination of low-dose μ receptor antagonist with κ receptor agonist was higher than the combination of middle-dose.
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