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作 者:黄晓玲[1] 邹毅[1] 单文燕[1] 潘冰冰[1] 孔高茵[1] 黄东[2]
机构地区:[1]湖南省人民医院麻醉科,长沙410005 [2]中南大学湘雅三医院,长沙410013
出 处:《中国疼痛医学杂志》2016年第9期655-658,共4页Chinese Journal of Pain Medicine
基 金:湖南省卫生厅科技计划项目(B2011-074)
摘 要:目的:探讨右美托咪定(dexmedetomidine,Dex)对瑞芬太尼(remifentanil,Ren)诱发的术后痛觉过敏大鼠脊髓p38丝裂原活化蛋白激酶(p38MAPK)表达的影响。方法:雄性SD大鼠60只,随机分为5组,每组12只:对照组(C组);切口痛组(I组);切口痛+Ren组(R组),输注Ren(l.0μg/kg)4 h;切口痛+Ren+大剂量Dex组(RD1组),输注Ren(l.0μg/kg)4 h的同时给予Dex 10μg/kg负荷量,再以10μg/kg持续输注4 h;切口痛+Ren+常规剂量Dex组(RD2组),输注Ren(l.0μg/kg)4 h的同时给予Dex 5μg/kg负荷量,再以5μg/kg持续输注4 h。于术前24 h,停药后2 h、6 h、24 h和48 h(T0-T4时点)以累积疼痛评分(CPS)评估大鼠疼痛强度。最后取大鼠腰段脊髓行免疫组织化学检测,观察p38MAPK的表达。结果:R组在T3-T4时点的CPS值较I组明显升高(P<0.05),而RD1组与RD2组在T1-T4时点的CPS值明显低于R组与I组(P<0.05),RD1组与RD2组组间CPS值相比无显著差异;R组p38MAPK染色实际灰度为132.83±7.32,显著高于其它各组(P<0.01);RD1组为69.87±6.17,RD2组74.57±7.11,均显著低于I组(91.43±5.76)(P<0.05),而RD1与RD2两组之间相比差异不显著(P>0.05),与C组(57.56±3.44)比较亦无统计学意义。结论:右美托咪定预防瑞芬太尼诱发的术后痛觉过敏机制与抑制脊髓p38MAPK表达有关,且与剂量无关。Objective: To investigate the effect of dexmedetomidine(Dex) on the activation of spinal p38 mitogen protein kinase in remifentanil(Ren) induced postoperative hyperalgesia rats. Methods: Sixty adult, male SD rats were randomly divided into five groups with twelve rats in each: Control group(C); Incision pain group(I); Remifentanil group(R): rats were given intravenous remifentanil l.0 μg/kg continuously for 4 h; Large dosage of Dex group(RD1): remifentanil was given the same dose of group R, meanwhile Dex was given at a rate of 10 μg/kg for 4 h after a loading dose of Dex10 μg/kg; Regular dosage of Dex group(RD2): remifentanil was given the same dose of group R, meanwhile Dex was given at a rate of 5 μg/kg for 4 h after a loading dose of Dex 5 μg/kg. Incisions were made in all rats except those in group C. Cumulative pain score(CPS) was measured 24 h before plantar incision and 2, 6, 24 and 48 h after drug withdrawal. P38 MAPK positive cells in the spinal cord were examined using immunohistochemistry method. Results: The CPS of group R at T3-T4 was significantly higher than those of group I; The CPS of group RD1 and RD2 were significantly lower than those of group I and group R. There was no significant difference between RD1 and RD2. The actual gray density of p38 MAPK in group R(132.83±7.32) was significantly increased than that of the rest groups. The p38 MAPK expression in both group RD1(69.87±6.17) and RD2(74.57±7.11) were significantly lower than that of group I(91.43±5.76), but there was no significant difference between these two groups, and did not have significant difference with group C(57.56±3.44). Conclusion: Dex could prevent remifentanil induced hyperalgesia due to the inhibition of p38 MAPK in the spinal cord. There was no difference between a regular and a large dosage of Dex.
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