| Objective:Animal models of reperfusion and ischemia separation can be established by insertion of a balloon catheter into the spinal canal to mimic human acute spinal injury. This study is aimed to explore the effects of different ischemia time windows on spinal injury of rats using biochemical and immunohistochemical methods.Methods:Thirty-six Sprague-Dawley rats were randomly divided into six groups, including sham group(C0), ischemia 10 minutes (C1), ischemia 30 minutes (C2), ischemia 45 minutes (C3), ischemia 60 minutes (C4), ischemia 90 minutes (C5). All rats were treated with corresponding time of ischemia, and reperfused for 48 hours. The neurological functional status of animal was assessed with the modified Tarlov grading, at the moment of revival 48h after the reperfusion. After last scoring, the thoracic segments of spinal cord were removed for pathological examination, biochemical and immunohistochemical analysis.Results:After 48 hours of reperfusion, with the elongation of ischemia time, spinal cord anterior horn neuron necrosis and apoptosis was gradually aggravated, malondialdehyde(MDA) level was gradually increased, superoxide dismutase(SOD) activity was gradually decreased, and rat neuroethological symptoms was aggravated.Conclusion:The rat model of ischemia-reperfusion injury is successfully established using a balloon catheter, and the injury of the spinal cords was deteriorated increasingly with the elongation of the ischemia time. The safe clamping duration without spinal cord injury is not more than 30 min at normothermia. |
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