Objective：To evaluate the effect of dexmedetomidine on ischemia/reperfusion-induced mitochondrial injury in a rat ex vivo lung model. Methods：Sprague-Dawley rats were randomly divided into four groups（n=6 each）：control group（group C），ischemia/reperfusion group（group IR），1 nmol/L of dexmedetomidine group（group D1）and 10 nmol/L of dexmedetomidine group（group D10）. An interleukin 2（IL-2）ex vivo lung perfusion system was used to establish a rat lung model of ischemia-reperfusion injury. Airway pressure（Raw），lung compliance（Cdyn），perfusion flow（VT）and pulmonary venous oxygen partial pressure（PaO2）were recorded at four points in time：the end of balance（T0），0 min（T1），30 min（T2）and 60 min（T3）of reperfusion. Lung injury was assessed by histopathological changes and lung wet/dry（W/D）weight ratio. The levels of lactate dehydrogenase（LDH），superoxide dismutase（SOD），malondialdehyde（MDA），reactive oxygen species（ROS），and adenosine triphosphate（ATP）were measured. Mitochondrial swelling and mitochondrial membrane potential（MMP）were measured. Results：Compared with group C，the pulmonary function of group IR，D1，and D10 worsened. LDH activity increased，as well as the content of ROS and MDA. SOD activity and the production of ATP decreased. The level of mitochondrial swelling increased，and mitochondrial MMP decreased in group D1 and D10（P < 0.05）. Compared with group IR，the pulmonary function of group D1 and D10 was improved，and pathological changes showed that lung injury was significantly reduced. The activity of LDH decreased，content of ROS and MDA decreased，SOD activity and ATP production increased，mitochondrial swelling decreased，MMP increased（P < 0.05）. Compared with group D1，the pulmonary function of group D10 was improved，Raw and LDH activity decreased while SOD activity increased，and mitochondrial swelling reduced（P < 0.05）. Conclusion：Dexmedetomidine can alleviate lung ischemia/reperfusion injury in a rat ex vivo lung model，and the mechanism may be related to alleviating mitochondrial injury and oxidative stress.