摘要目的 评价瑞芬太尼诱发切口痛大鼠痛觉过敏时脊髓趋化因子配体3 (CCL3)和趋化因子CC亚族受体5(CCRS)表达水平的变化.方法 雄性SD大鼠32只,体重240～ 260 g,2～3月龄,采用随机数字表法,分为4组(n=8):对照组(C组)、切口痛组(I组)、瑞芬太尼组(R组)和瑞芬太尼+切口痛组(R+I组).于切口痛模型制备的同时静脉输注瑞芬太尼1μg·kg-1 ·min-1,输注时间60 min,分别于输注瑞芬太尼前24 h(基础状态)、输注停止后2、6、24和48 h测定机械缩足反应阈(MWT)和热缩足潜伏期(TWL),最后一次测定痛阈后处死大鼠,取脊髓L4-6节段,采用荧光定量PCR法测定CCL3 mRNA和CCR5 mRNA的表达水平,采用Western blot法测定CCL3和CCR5的表达水平.结果 与C组比较,I组、R组和R+I组MWT降低,TWL缩短,脊髓CCL3 rmRNA和CCR5 mRNA及其蛋白表达上调(P＜0.05);与I组和R组比较,R+I组MWT降低,TWL缩短,脊髓CCL3 mRNA和CCR5 mRNA及其蛋白表达上调(P＜0.05).结论 瑞芬太尼诱发切口痛大鼠痛觉过敏形成的机制与脊髓CCL3和CCR5表达上调有关.

abstractsObjective To evaluate the changes in the expression of CC-chemokine ligand 3 (CCL3) and CC-chemokine receptor 5 (CCR5) in the spinal cord during hyperalgesia induced by remifentanil in rats with incisional pain.Methods Thirty-two male Sprague-Dawley rats,aged 2-3 months,weighing 240-260 g,were randomly divided into 4 groups (n=8 each) using a random number table:control group (group C),incisional pain group (group Ⅰ),remifentanil group (group R) and remifentanil+incisional pain group (group R+I).A 1-cm longitudinal incision was made in the plantar surface of the left hindpaw in anesthetized rats.While the model of incisional pain was established,remifentanil was infused for 60 min at 1 μg · kg-1 · min-1.At 24 h before infusion of remifentanil (baseline) and 2,6,24 and 48 h after the end of infusion,the mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) were measured.The rats were sacrificed after the last measurement of pain threshold,the lumbar segment (L4-6) of the spinal cord was removed for determination of CL3 and CCR5 mRNA expression (by real-time PCR) and CL3 and CCR5 expression (by Western blot).Results Compared with group C,the MWT was significantly decreased,the TWL was shortened,and the expression of CCL3 and CCR5 mRNA and protein was up-regulated in I,R and R+ I groups.Compared with I and R groups,the MWT was significantly dccreascd,the TWL was shortened,and the expression of CCL3 and CCR5 mRNA and protein was up-regulated in group R+I.Conclusion The mechanism by which remifentanil induces hyperalgesia is related to up-regulated expression of CCL3 and CCR5 in the spinal cord of rats with incisional pain.