DEXMEDETOMIDINE ATTENUATES SPINAL CORD ISCHEMIA-REPERFUSION IN RATS BY INHIBITING PROINFLAMMATORY FACTORS AND ATTENUATING LIPID PEROXIDATION IN SPINAL CORD TISSUE

Xinping Yang^{1, #}, Han Yang^{1, #}, Yongqiang Zhan^{2, *}, Jie Zhang¹, Zhiheng Liu¹

¹Department of Anesthesiology, the First Affiliated Hospital of Shenzhen University; The Second People’s Hospital of Shenzhen, Shenzhen, 518035 - ²Department of Surgery, the First Affiliated Hospital of Shenzhen University; The Second People’s Hospital of Shenzhen, Shenzhen, 518035

Objective: To study the mechanism through which dexmedetomidine alleviates spinal cord ischemia-reperfusion in rats. 

Methods: A total of 72 clean, healthy, male Sprague-Dawley (SD) rats were randomly selected and divided into three groups containing 24 rats each: sham operation group, model group, and dexmedetomidine group. The spinal cord ischemia-reperfusion rat model was established. Rats in the sham operation group only underwent laparotomy and threading. Rats in the dexmedetomidine group were given a tail-vein injection of 4 µg/kg dexmedetomidine. The Tarlov score was used to evaluate the neurobehavioral functions of rats at each time point. Hematoxylin and eosin (HE) staining was used to determine the pathological changes in the spinal cords of rats. Enzyme-linked immunosorbent assay (ELISA) was used to determine the levels of tumor necrosis factor-α (TNF-α) and interleukin-1α (IL-1α) in the spinal cord tissue of rats from each group. The xanthine oxidation method was used to determine changes in superoxide dismutase (SOD) activity, and the thiobarbital method was used to determine the levels of malondialdehyde (MDA) in rats from each group. The number of normal neurons in the anterior horn of the spinal cord was observed by microscope. 

Results: Compared with the sham operation group, the Tarlov score, SOD levels, and the number of normal neurons in the anterior spinal horn of rats in the model group were significantly reduced, and the levels of TNF-α, IL-1α, and MDA were significantly increased (P<0.05). Compared with the model group, the Tarlov score, SOD levels, and the number of normal neurons in the anterior horn of the spinal cord in the dexmedetomidine group were significantly increased, and the levels of TNF-α, IL-1α, and MDA were significantly reduced (P<0.05). The nerve cells in the sham operation group presented clear outlines, the cytoplasm contained the same distribution of Nissl bodies, the nuclear morphological structure was typical, and the nucleoli were large and obvious. In contrast, the neuronal contours of the rats in the model group disappeared or were unclear; the cytoplasm of the rats was indifferent, the nuclear morphology was abnormal, and the nucleoli were reduced or disappeared. The contours of the nerve cells in the dexmedetomidine group disappeared, with slight edema, and some of the cytoplasmic and nucleoli morphology were blurred. 

Conclusion: Dexmedetomidine can significantly reduce spinal cord ischemia-reperfusion injury and improve neurological function in rats, which may be associated with the inhibition of pro-inflammatory factors and the reduction of lipid peroxidation in spinal cord tissue.