• Wan-Wei Jiang, Qing-Hui Wang, Ya-Jing Liao, Pai Peng, Min Xu, and Li-Xin Yin.
• Department of Anesthesiology II, Affiliated Zhongshan Hospital of Dalian University, No. 6 of Jiefang Street, Zhongshan District, Dalian, 116001, China. wanweijdoc@163.com.
• BMC Anesthesiol. 2017 Sep 20; 17 (1): 130.

BackgroundDexmedetomidine is a highly selective adrenergic receptor agonist, which has a dose-dependent sedative hypnotic effect. Furthermore, it also has pharmacological properties, and the ability to inhibit sympathetic activity and improve cardiovascular stability during an operation. However, its protective effect on patients with severe craniocerebral injury in the perioperative period remains unclear.MethodEighty adult male SD rats were used and divided into two groups (n = 40, each group): dexmedetomidine injury group (experimental group), and sodium chloride injury group (control group). Models of severe craniocerebral injury were established in these two groups using the modified Feeney's free-fall method. As soon as the establishment of models was succeed, rat in the experimental group received 1 μg of dexmedetomidine (0.1 ml), while each rat in the control group was given 0.1 ml of 0.9% sodium chloride. Blood was sampled from an incision at the femoral vein to detect TNF-α and IL-2 levels at 1, 12, 24,36,48 and 72 h after establishing the model in the two groups.ResultsAfter severe craniocerebral injury, TNF-α levels of rats were lower in every stage and at different degrees in the experimental group than in the control group (P < 0.05), while IL-2 levels were lower in the experimental group to different extents (P < 0.05).ConclusionDexmedetomidine protects the brain of rats with severe craniocerebral injury by reducing the release of inflammatory mediators.

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