高压氧对家兔急性脊髓缺血再灌注损伤的保护作用

目的　通过建立兔脊髓缺血再灌注损伤模型观察其组织病理学、生化指标及影像学变化，探讨脊髓缺血再灌注损伤机制。在此基础上研究高压氧对脊髓缺血损伤的保护作用。方法　采用夹闭法制备家兔急性脊髓缺血再灌注损伤模型，测定脊髓缺血４０ 分钟及再灌注后脂质过氧化物（ＬＰＯ）含量以及超氧化物歧化酶（ＳＯＤ） 活性，并观察神经功能缺失程度及组织病理学变化，同时观察腰（Ｌ４）为中心脊髓磁共振扫描（ＭＲＩ）的变化。结果　脊髓缺血４０ 分钟后所有动物均出现双后肢瘫痪，肌力为２ 级，再灌注后动物神经功能有不同程度的恢复；缺血后脊髓组织ＬＰＯ 含量明显升高，ＳＯＤ活性下降，与正常对照及假手术组相比差异有显著性（ Ｐ＜０ ．０５），再灌注后ＬＰＯ 含量有所下降，直至２４ 小时恢复正常，ＳＯＤ 则在再灌注２～６ 小时活性进一步降低，至２４ 小时恢复正常水平。组织病理学显示缺血后即有明确的病理改变，再灌注后这种改变更为严重；ＭＲＩ显示脊髓缺血后Ｔ２ 加权像有明确的异常高信号；ＨＢＯ 治疗组与缺血再灌注６ 小时对照组相比较，ＬＰＯ含量下降，ＳＯＤ活性增强，差异有显著性（ Ｐ＜０ ．０５）。结论　脂质过氧化是脊髓缺血再灌注损伤的主要机制，高压氧治疗可增强自由基清除

Protection of hyperbaric oxygenation for acute ischemic spinal cord re-perfusion injury in rabbits

Objective Based on a change of histopathology,biochemistry and MRI in rabbit models of acute ischemic spinal cord re-perfusion injury,the spinal injuried mechanism and protection of hyperbaric oxygenation(HBO) on spinal ischemic injury were studied.Methods The rabbit models of spinal cord ischemic injury were formed by occlusion of abdominal aorta in rabbits.After 40 min of spinal ischemia and re-perfusion,the lipid peroxide(LPO) level and superoxide dismutase(SOD) activity were measured;the disappeared degrees of denervation function,histopathology and MRI(L4 centrically) were observed,too.Results At post-spinal cord ischemia of 40 min,all animals got paralysis in their hind limbs(muscle-force II);LPO level raised and SOD activity reduced obviously,when compared with the normal control group(P<0.05).The changes were returned to normal after 24h of re-perfusion.The abnormal alterations of histopathology and MRI were found in spinal ischemia period,particularly in re-perfusion.These experimental rabbits were treated with HBO therapy(inhaled 99.5% O 2,0.2 MPa,40 min).Result showed that LPO level decreased and SOD activity enhanced,there was a marked difference(P<0.05). Conclusion It suggests that LPO is a main mechanism of spinal cord ischemia and re-perfusion injury.HBO therapy may enhance the SOD activity and reduce the formation of free radicals.So HBO has a protection against the acute ischemic spinal cord re-perfusion injury.