论文部分内容阅读
目的 探讨鞘内注射曲马多抗伤害性效应及与脊髓α_2受体效应的关系。方法 Wistar大鼠蛛网膜下腔埋管后随机分为5组(n=8):生理盐水对照组、曲马多10μg组、育亨宾10μg组、育亨宾1mμg+曲马多10μg组。育亨宾10μ+纳洛酮10μg+曲马多10μg组。于大鼠左后爪掌心皮下注射2.5％福尔马林50μl后鞘内注入上述药物,从福尔马林注射后的30min开始对大鼠的表现行为进行Dubuisson ＆ Dennis评分。另取一组大鼠断头处死后取腰段脊髓制成细胞膜悬液,以~3H-育亨宾为放射性标记配基,盐酸育亨宾为非标记配基,曲马多为竞争剂,行标记配基的饱和结合反应及竞争取代反应,并计算~3H-育亨宾与脊髓α_2受体结合的平衡解离常数(KD)及曲马多与~3H-育亨宾竞争结合脊髓α_2。受体的抑制常数(KI)。结果 鞘内注入10μg的曲马多能显著抑制福尔马林注射后大鼠的疼痛反应。10μg育亨宾单独鞘内注入无明显抗伤害性效应(P>0.05),预处理可使10μg曲马多鞘内注入后大鼠的伤害效应评分最多可增加56%,但仍低于对照组大鼠的伤害性效应评分(P<0.05);增加纳洛酮10μg预处理可使10μg曲马多鞘内注入后大鼠的伤害效应评分增加200％。受体放射性分析表明~3H-育亨宾的KD值为1.79nmol/L,曲马多的KI值为34.14μmol/L,IC_(50)为68.25μmol/L,提示曲马多与
Objective To investigate the anti-nociceptive effect of intrathecal tramadol and its relationship with the α 2 -receptor effect of spinal cord. Methods Wistar rats were randomly divided into 5 groups (n = 8): normal saline control group, tramadol 10μg group, yohimbine 10μg group, yohimbine 1mμg + tramadol group 10μg. Yohimbin 10μ + naloxone 10μg + tramadol 10μg group. The rats were injected subcutaneously with 2.5% formalin (50μl) into the palm of the left hindpaw and received the Dubuisson & Dennis score 30 minutes after the formalin injection. Another group of rats were sacrificed after decapitation to take the lumbar spinal cord membrane suspension made of ~ 3H-yohimbe for radiolabeled ligand, yohimbe hydrochloride non-labeled ligand, tramadol as a competitor, Saturation binding reaction and competitive substitution reaction of labeled ligand were performed. The equilibrium dissociation constants (KD) of ~ 3H-yohimbine and spinal cord α 2 receptor binding were calculated, and the interaction between tramadol and ~ 3H-yohimbine in combination with spinal α 2 . Receptor inhibition constant (KI). Results Intrathecal injection of 10 μg of tramadol significantly inhibited the pain response in rats after formalin injection. 10μg yohimbine alone intrathecal injection had no significant anti-nociceptive effect (P> 0.05), pretreatment can make 10μg tramadol intrathecal injection injury scores up to 56%, but still lower than the control group (P <0.05). The pretreatment with 10μg naloxone could increase the damage effect score of rats by 10% after intrathecal injection of 10μg tramadol by 200%. Radioimmunoassay showed that the KD value of ~ 3H-yohimbine was 1.79nmol / L, that of tramadol was 34.14μmol / L, and that of IC 50 was 68.25μmol / L, suggesting that tramadol