肢体缺血预处理对兔颈髓慢性缺血后再灌注损伤的影响

The effect of limb ischemic preconditioning on reperfusion injury of spinal cord after chronic ischemic in rabbit

目的:探讨肢体缺血预处理对兔颈髓慢性缺血后再灌注损伤的影响及其机制。方法:建立兔颈髓慢性压迫损伤模型,随机分为实验组和对照组。实验组在脊髓减压再灌注前给予肢体缺血预处理,对照组不做预处理。两组兔在减压前和减压后2h、8h、24h,7d、21d分别进行后肢神经功能评分。在减压后即刻、0.5h、1h和以上时间点分别进行脊髓血流测定。处死动物取脊髓(C1～T1)进行组织病理学检查。结果:实验组于再灌注8h后神经功能评分明显好于对照组。实验组脊髓组织丙二醛含量于再灌注8h后显著低于对照组。两组再灌注后脊髓血流均显著下降,实验组优于对照组。病理学检查示对照组神经元呈缺血改变,白质水肿、脱髓鞘;实验组病理改变轻微。实验组热休克蛋白70表达阳性,对照组为阴性。结论:肢体缺血预处理对脊髓慢性缺血后的再灌注损伤具有明显保护作用。

Objective:To investigate the effect and mechanism of limb ischemic preconditioning (IP) on reperfusion injury of spinal cord following chronic ischemic in rabbit models.Method:The rabbit model of chronic compression myelopathy was made under the monitoring of cerebral somatosensory evoked potential(CSEP).Rabbit models were randomly divided into control group and experimental group.Before decompression,limb ischemic preconditioning(LIP) was performed in experimental group while direct decompression in control group.All rabbits were evaluated based on their Tarlov criteria before decompression and at 2 hours,8 hours,24 hours,7 days and 21days after decompression.Spinal cord blood flow(SCBF) was scaled immediately,at 0.5 hour,1 hour and above time point after decompression.Following these processes,all rabbits were sacrificed,spinal cords(C1-T1) were harvested immediately for histopathologic test.Result:Hind limbs,function scores in the experimental group was higher than that in control group after 8h′s reperfusion.MDA content of spinal cord in experimental group was significantly lower than that in controlled group after 8h′s reperfusion.SCBF decreased remarkably in both two groups after reperfusion with experimental group less than control group.Histopathological test showed neurons′ ischemic property,glial cell proliferation,neurs′ phagocytosis in control group,while little change in the experimental group.Heat shock protein 70(HSP70) staining was positive in experimental group,while negative all the time in the control group.Conclusion:Endogenic protective mechanism evoked by LIP can obviously prevent reperfusion injury of spinal cord following chronic ischemic in experimental animal model.