中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2015年
3期
326-329
,共4页
李楠%张麟临%舒瑞辰%王志芬%丁玲%敖吉莹%王国林
李楠%張麟臨%舒瑞辰%王誌芬%丁玲%敖吉瑩%王國林
리남%장린림%서서신%왕지분%정령%오길형%왕국림
哌啶类%痛觉过敏%疼痛%趋化因子CCL3%受体,CCR5%脊髓
哌啶類%痛覺過敏%疼痛%趨化因子CCL3%受體,CCR5%脊髓
고정류%통각과민%동통%추화인자CCL3%수체,CCR5%척수
Piperidines%Hyperalgesia%Pain%Chemokine CCL3%Receptors,CCR5%Spinal cord
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.
目的 評價瑞芬太尼誘髮切口痛大鼠痛覺過敏時脊髓趨化因子配體3 (CCL3)和趨化因子CC亞族受體5(CCRS)錶達水平的變化.方法 雄性SD大鼠32隻,體重240～ 260 g,2～3月齡,採用隨機數字錶法,分為4組(n=8):對照組(C組)、切口痛組(I組)、瑞芬太尼組(R組)和瑞芬太尼+切口痛組(R+I組).于切口痛模型製備的同時靜脈輸註瑞芬太尼1μg·kg-1 ·min-1,輸註時間60 min,分彆于輸註瑞芬太尼前24 h(基礎狀態)、輸註停止後2、6、24和48 h測定機械縮足反應閾(MWT)和熱縮足潛伏期(TWL),最後一次測定痛閾後處死大鼠,取脊髓L4-6節段,採用熒光定量PCR法測定CCL3 mRNA和CCR5 mRNA的錶達水平,採用Western blot法測定CCL3和CCR5的錶達水平.結果 與C組比較,I組、R組和R+I組MWT降低,TWL縮短,脊髓CCL3 rmRNA和CCR5 mRNA及其蛋白錶達上調(P＜0.05);與I組和R組比較,R+I組MWT降低,TWL縮短,脊髓CCL3 mRNA和CCR5 mRNA及其蛋白錶達上調(P＜0.05).結論 瑞芬太尼誘髮切口痛大鼠痛覺過敏形成的機製與脊髓CCL3和CCR5錶達上調有關.
목적 평개서분태니유발절구통대서통각과민시척수추화인자배체3 (CCL3)화추화인자CC아족수체5(CCRS)표체수평적변화.방법 웅성SD대서32지,체중240～ 260 g,2～3월령,채용수궤수자표법,분위4조(n=8):대조조(C조)、절구통조(I조)、서분태니조(R조)화서분태니+절구통조(R+I조).우절구통모형제비적동시정맥수주서분태니1μg·kg-1 ·min-1,수주시간60 min,분별우수주서분태니전24 h(기출상태)、수주정지후2、6、24화48 h측정궤계축족반응역(MWT)화열축족잠복기(TWL),최후일차측정통역후처사대서,취척수L4-6절단,채용형광정량PCR법측정CCL3 mRNA화CCR5 mRNA적표체수평,채용Western blot법측정CCL3화CCR5적표체수평.결과 여C조비교,I조、R조화R+I조MWT강저,TWL축단,척수CCL3 rmRNA화CCR5 mRNA급기단백표체상조(P＜0.05);여I조화R조비교,R+I조MWT강저,TWL축단,척수CCL3 mRNA화CCR5 mRNA급기단백표체상조(P＜0.05).결론 서분태니유발절구통대서통각과민형성적궤제여척수CCL3화CCR5표체상조유관.
Objective 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.
