• Bing-Qian Xiang, Jin-Bo He, Hui Gao, Zi-Yin Luo, Yong-Yue Dai, and Wan-Tie Wang.
• Institute of Ischemia/Reperfusion Injury, Wenzhou Medical University, Wenzhou 325035.
• Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2017 May 8; 33 (5): 415-419.

ObjectiveTo evaluate the effects and mechanism of the Dexmedetomidine on the levels of proinflammatory mediators interleukin 1 beta (IL-1β) and tumor necrosis factor-α(TNF-α) in ischemia/reperfusion(I/R)rats.MethodsFifty healthy SPF male SD rats, 250~310 g,8~12 weeks,were randomly divided into five groups(n=10):sham operation group(sham group),I/R group, dexmedetomidine group(Dex group), atipamezole group(Atip group), dexmedetomidine plus atipamezole(Dex+Atip group). The I/R model was established by clipping hilus of left lung for 30 min and then reperfusion for 2 h. Dex group, Atip group and Dex + Atip group were performed by intraperitoneal injection dexmedetomidine(20 μg/kg),atipamezole(250 μg/kg),Dexmedetomidine(20 μg/kg)+atipamezole(250 μg/kg)respectively 30 min in advance before hilus of left lung was clipped, the rest of the process was the same with I/R group. After the experiment the rats were killed and the left lung tissues to determine the lung wet/dry weight(W/D) and total lung water content(TLW); Ultra structure of lung tissues were observed under light microscope and electron microscope; IL-1β and TNF-α levels were determined by using ELISA.ResultsCompared with the sham group, the W/D、TLW、IL-1β and TNF-α in other groups were increased significantly (P<0.05). The structure damages of lung tissues observed under light microscope and electron microscope in other groups were more serious than that of sham group. Compared with I/R、Atip、Dex+Atip group, the levels of W/D、TLW,IL-1β and TNF-α in Dex group were lower (P<0.05), the structure damages of lung tissues observed under light microscopy and electron microscope in Dex group were slighter. There was no significant difference of the above parameters among I/R、Atip、Dex+Atip group.ConclusionsDexmedetomidine can alleviate ischemia/reperfusion injury in rat lung through lowering the level of proinflammatory mediators IL-1β and TNF-α,the possible mechanism may be through stimulation of α2 adrenaline receptors.

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