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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 the effect of dexmedetomidine on the expression of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) during spinal cord ischemia-reperfusion injury in rabbits. Methods Twenty-four New Zealand white rabbits were selected and randomly divided into experimental group, model group and sham operation group (all n = 8). Spinal cord ischemia-reperfusion model was established in rabbits. 30 min before ischemia, dexmedetomidine 2.5μg · kg -1 was infused intravenously in experimental group until reperfusion. The rats in model group were injected with normal saline At 6, 12, 24 and 48 hours after perfusion, the motor function of hindlimbs was evaluated by Tarlov method. The levels of TNF-α and IL-1β in serum were also measured at 6, 12, 24 and 48 h after operation The levels of TNF-α, IL-1β, superoxide dismutase (SOD) and malondialdehyde (MDA) in the spinal cord of each rabbit were measured 48 h later. The pathological changes were observed by HE staining. Results Compared with the sham operation group, the Tarlov score of the model group and the experimental group decreased significantly at each time point. The levels of TNF-α and IL-1β were significantly increased in the serum and spinal cord, the content of MDA in the spinal cord was significantly increased, and the content of SOD in the spinal cord was decreased significantly (all P <0.05) . Compared with the model group, the Tarlov score at each time point in the experimental group was significantly increased, the levels of TNF-α and L-1β in the serum and spinal cord were significantly decreased, the content of MDA in the spinal cord was significantly decreased, SOD in the spinal cord was significantly increased (all P <0.05) Obviously relieved. Conclusion Dexmedetomidine can reduce the injury of spinal cord ischemia-reperfusion in rabbits. The mechanism may be related to the inhibition of proinflammatory cytokines.