右美托咪定对兔脊髓缺血再灌注损伤促炎性因子表达的影响  

Effects of dexmedetomidine on spinal cord ischemia-reperfusion injury in rabbits proinflammatory cytokine expression

作　　者：吕少君[1,2] 翁浩[2] 刘海健[2] 齐乐[2] 徐志勇[2] 刘荣[2] 黄丁丁[2] 

机构地区：[1]南方医科大学附属第三临床医学院,广州510515 [2]南方医科大学附属奉贤医院麻醉科,上海201400

出　　处：《中国临床药理学杂志》2016年第6期553-556,共4页The Chinese Journal of Clinical Pharmacology

摘　　要：目的评价右美托咪定对兔脊髓缺血再灌注损伤时促炎性因子肿瘤坏死因子α(TNF-α)、白细胞介素-1β(IL-1β)的影响。方法选取新西兰大白兔24只,用随机数字表法分为实验组、模型组、假手术组(均n=8)。建立兔脊髓缺血再灌注模型,缺血之前30 min,实验组开始静脉输注右美托咪定2.5μg·kg^(-1)直至再灌注;模型组泵入等量的生理盐水;再灌注后6,12,24,48 h,用Tarlov法评价兔后肢的运动功能,并同时检测各组手术前及再灌注后6,12,24,48 h血清TNF-α、IL-1β的表达水平;48 h后取各只兔脊髓,检测TNF-α、IL-1β、超氧化物歧化酶(SOD)和丙二醛(MDA)水平表达,并作HE染色观察病理变化。结果与假手术组比较,模型组和实验组各个时间点Tarlov评分明显降低,血清和脊髓TNF-α、IL-1β明显升高,脊髓MDA明显升高,脊髓SOD明显降低(均P<0.05)。与模型组比较,实验组各个时间点Tarlov评分明显升高,血清和脊髓TNF-α、L-1β明显降低,脊髓MDA明显降低,脊髓SOD明显升高(均P<0.05),HE染色病理损伤明显减轻。结论右美托咪定能减轻兔脊髓缺血再灌注的损伤,其机制可能与抑制促炎因子有关。Objective To evaluate of dexmedetomidine in rabbit spinal cord ischemia reperfusion injury proinflammatory cytokine tumor necrosis factor-α（ TNF-α）,interleukin-1β（ IL-1β） effect. Methods Twenty-four New Zealand white rabbits were randomly divided into three groups： sham operated group（ n = 8）,model group（ n = 8） and experimental group（ n = 8）. The rabbit spinal cord ischemia again perfusion model was established,before ischemia 30 min vein infusion of dexmedetomidine 2. 5 μg·kg^（-1）until reperfusion before in experimental group.The model group and sham operation group,and the same time was pumped into the same amount of normal saline. After reperfusion,6,12,24 and 48 h were used to evaluate the motor function of the hind limbs of the rabbits by Tarlov method. The expression levels of TNF-α,IL-1βat the time of 6,12,24,48 h were detected after surgery. The TNF-α,IL-1β,superoxide dismutase（ SOD） and malondialdehyde（ MDA）were detected and the pathological changes were observed by HE staining and 48 h staining. Results Compared with the sham operation group,the Tarlov score of the model group and the experimental group wasdecreased,serum and spinal cord TNF-α,IL-1β increased,MDA,SOD decreased（ all P〈0. 05）,HE staining pathological damage aggravated. Compared with the model group,the Tarlov score of the experimental group was higher,serum and spinal cord TNF--α,IL-1β decreased,spinal cord MDA and SOD decreased（ all P〈0. 05）. The pathological damage of HE staining was decreased. Conclusion Dexmedetomidine can alleviate the rabbit spinal cord ischemia reperfusion injury,its mechanism may be associated with proinflammatory factor.

关 键 词：右美托咪定 脊髓 缺血再灌注损伤 白细胞介素-1Β 肿瘤坏死因子-Α 

分 类 号：R969.1[医药卫生—药理学]