Effects Of Hyperoxygen Lipuid On Spinal Cord Injury Induced By Ischemia And Reperfusion In Rabbits

Objective: To investigate the protective effects and mechanisms of hyperoxygen liquid on spinal cord ischemia reperfusion injury, providing the theoretic base for hyperoxygen liquid to treat the neuronal ischemic injury.Methods: Twenty-four male New Zealand white rabbits were randomly divided into four groups: Control group 1 (Ci, n=6), Control group 2 (C2, n=6); Hyperoxygen liquid group 1 (Hi, n=6) and Hyperoxygen liquid group 2(H2, n=6). The spinal cord ischemia rabbit model was made by occluding infrarenal abdominal aorta for 20min. In Group HI, hyperoxygen liquid was administered intravenously 30min before clamping at the rate of 5ml?kg-1 ?k-1. In Group H2, hyperoxygen liquid was administered epidurally 30min before clamping at the rate of 5ml ?kg-1 ?k-1 In Group Ci and C2, saline was used as Group HI and H2, respectively. The level of plasma TXB2 and the 6-keto-PGFi a were assayed 20min before ischemia, l0min after ischemia and 20min after reperfusion. Neurologic at status was scored at 4, 8, 12, 24 and 48 h after reperfusion. All animals were killed at 48h after reperfusion, the expression of HSP 90 was study using immunohistochemical staining in conjunction with histopathological analysis of ischemic spinal cords.Results: At the timepoints of 4, 8, 12, 24 and 48h after reperfusion,-4-animals in group H (which received hyperoxygen liquid) showed a significantly higher neurological function scores compared with those in control group. Hyperoxygen liquid markedly injury attenuated the degree of ischemic/reperfusion destruction in spinal cord neurons and decreased the number of destroyed neurons. The serum concentration of TXB2N and MDA were lower than that of group C₁ and C₂, while the activity of 6-Keto-PGF1a? SOD and expression of HSP90 in group H were proved to be higher than that of control groups.Conclusion: Hyperoxygen liquid showed significantly protective effect to ischemia/ reperfusion injury in rabbits. The possible mechanism referred to its ability to protect the activity of SOD and 6-Keto-PGF1a, to increase the expression of HSP90, and to decrease the serum concentration of TXB2 and MDA.