论文部分内容阅读
目的:观察瑞芬太尼对切口痛大鼠脊髓诱导型一氧化氮合酶(i NOS)mRNA及FOS蛋白表达的影响,探讨瑞芬太尼诱发痛觉过敏的可能机制。方法:48只SD大鼠随机分为4组(n=12):对照组(C组),切口痛组(I组),瑞芬太尼1组(R1组),瑞芬太尼2组(R2组)。分别于术前24 h(基础值),术后24,48 h测定机械性痛阈。痛阈测定后,测定脊髓i NOS mRNA和FOS蛋白表达。结果:与术前24 h比较,术后I组、R1组和R2组机械痛阈降低;与C组比较,I组、R1组和R2组机械性痛阈降低;与I组比较,R1组和R2组机械性痛阈降低;与R1组比较,R2组机械性痛阈升高(P<0.05或P<0.01)。与C组比较,I组,R1组和R2组i NOS mRNA和FOS蛋白表达上调;与I组比较,R1和R2组i NOS mRNA和FOS蛋白表达上调;与R1组比较,R2组i NOS mRNA和FOS蛋白表达下调(P<0.05或P<0.01)。结论:瑞芬太尼可能通过上调切口痛大鼠脊髓i NOS mRNA和FOS蛋白表达而诱导痛觉过敏。
Objective: To observe the effect of remifentanil on the expression of iNOS mRNA and FOS protein in spinal cord tissue of rats with incisional pain and to explore the possible mechanism of remifentanil-induced hyperalgesia. Methods: Forty eight SD rats were randomly divided into 4 groups (n = 12): control group (C group), incision pain group (group I), remifentanil group 1 (R1 group), remifentanil group 2 (R2 group). Mechanical pain thresholds were measured at 24 h (baseline) and at 24 and 48 h postoperatively. After the pain threshold was measured, the spinal cord iNOS mRNA and FOS protein expression was measured. Results: Compared with 24 hours before operation, the mechanical pain threshold decreased in group I, group R1 and group R2; Compared with group C, mechanical pain threshold decreased in group I, group R1 and group R2; Compared with group I, group R1 And mechanical pain threshold of group R2 decreased. Compared with group R1, mechanical pain threshold of group R2 increased (P <0.05 or P <0.01). Compared with group C, the expression of iNOS mRNA and FOS protein were increased in group I, group R1 and group R2; Compared with group I, the expression of iNOS mRNA and FOS protein were increased in group R1 and R2; Compared with group R1, the expression of iNOS mRNA And FOS protein expression was down-regulated (P <0.05 or P <0.01). Conclusion: Remifentanil may induce hyperalgesia by up-regulating the expression of iNOS mRNA and FOS protein in spinal cord of incisional pain rats.