右美托咪啶对脓毒症大鼠血清炎性因子和氧化应激反应的影响

目的 探讨右美托咪啶对脓毒症大鼠血清炎性因子和氧化应激反应的影响.方法 健康雄性SD大鼠30只,10～ 14周龄,体重250～300 g,采用随机数字表法,将其随机分为3组(n=10):假手术组(S组)、脓毒症组(CLP组)和脓毒症+右美托咪啶组(CLP+D组).CLP组和CLP+D组采用盲肠结扎穿孔术制备脓毒症模型,CLP+D组术毕静脉输注右美托咪啶10 μg·kg-1·h-1至大鼠死亡或术后12 h,S组和CLP组给予等容量生理盐水1ml·kg-1·h-1.每组取5只大鼠,分别于术前(基础状态)、术后1、6、12 h时采集股动脉血样,测定血清IL-6、IL-10、SOD及MDA的水平.记录术后12 h内大鼠生存情况.结果 与S组比较,CLP组术后1、6、12 h时血清IL-6、IL-10和MDA的浓度升高,血清SOD活性和生存率降低(P＜0.05)；与CLP组比较,CLP+D组术后6、12 h时血清IL-6和MDA的浓度降低,术后12 h时血清SOD活性和生存率升高(P＜0.05).结论 右美托咪啶可以提高脓毒症大鼠的生存率,其机制与抑制炎性因子释放及氧化应激反应有关.

Effects of dexmedetomidine on serum inflammatory factor and oxidative stress response in septic rats

Objective To investigate the effects of dexmedetomidine on serum inflammatory factor and oxidative stress response in septic rats.Methods Thirty healthy male SD rats,aged 10-14 weeks,weighing 250-300 g,were randomly divided into 3 groups( n =10 each): sham operation group (group S),sepsis group (group CLP) and sepsis + dexmedetomidine group (group CLP + D).Sepsis was induced by cecal ligation and puncture in groups CLP and CLP + D.Group CLP + D received intravenous infusion of dexmedetomidine at 10 μg· kg- 1 ·h- 1 from the end of operation until dead or 12 h after operation.Groups S and CLP received equal volume of normal saline at 1 ml·kg-1 ·h-1.Arterial blood samples were taken from 5 rats in each group before (basline) and at 1,6 and 12 h after operation for determination of serum IL-6,IL-10,SOD and MDA levels.The survival rate within 12 h after operation was recorded.Results Compared with group S,serum IL-6,IL-10 and MDA concentrations at 1,6 and 12 h after operation were increased,while serum SOD activity at 1,6 and 12 h after operation and survival rate were decreased in group CLP ( P ＜ 0.05 ).Compared with group CLP,serum IL-6 and MDA concentrations at 6 and 12 h after operation were decreased,while serum SOD activity at 12 h after operation and survival rate were increased in group CLP + D ( P ＜ 0.05 ).Conclusion Dexmedetomidine can increase the survival rate of septic rats by inhibiting inflammatory factor release and oxidative stress response.