缺血预适应后脊髓区域血流的改变及其对脊髓功能的保护作用

目的：探讨缺血预适应对脊髓区域血流的影响及其对脊髓功能的保护作用。方法：采用放射介入球囊栓塞方法建立脊髓缺血动物模型，氢去除电极测定脊髓区域血流，脊髓诱发电位监测脊髓功能，研究缺血预适应对脊髓缺血的保护作用。结果：缺血预适应５分钟后，脊髓局部区域血流升高，是脊髓诱发电位改变的直接原因；而脊髓区域血流的改变，可能与缺血预适后，儿茶酚胺类神经递质含量轻度升高有关。脊髓不可逆缺血损害后，单胺类递质（ＮＥ，ＤＡ，５－ＨＴ）的严重升高，将造成脊髓血管痉挛、内皮细胞裂隙、多灶出血、坏死，而使脊髓功能受损。脊髓区域血流与脊髓功能的改变密切相关；缺血预适应后，脊髓区域血流的轻度升高以及再次不可逆缺血（３０分钟缺血）后脊髓区域血流的明显改善，是缺血预适应对脊髓功能保护作用的直接原因。结论：缺血预适应可改变脊髓区域血流，增加长时间不可逆缺血后脊髓区域血流并对不可逆脊髓缺血后的脊髓功能损害有明显而确定的保护作用。

Effect of ischemic preconditioning on spinal cord blood flow and evcked potentials

Objective: With the advent of the protection of ischemic preconditioning in myocardium, more and more attention was paid to the ischemic preconditioning in central nervous system (CNS) This study was to evaluate the protection of ischemic preconditioning to spinal cord ischemia. Methods:Interventional neuroradiological technique was employed to establish the spinal cord ischemia model in rabbit and the experimental study of the protection of ischemic preconditionmg to spinal cord ischemia was first available in the paper. Results: After 5 minutes ischemic preconditioning with 20 minutes reperfusion,the regional spinal cord blood flow (rSCBF) was increased, which may be correlated to the increase of catecholamine, especially NE which is in proportion to the cAMP and indicating the enhancement of the metablic activities of the spinal cord. After 30 minutes unreversible ischemia, the great increase of catecholamine caused vascular spasm, endotheliocyte fissure, mutiple hemorrhagic suffusion, necrosis, which would injury the spinal cord as a result. The light increase of the rSCBF and the amelioration of the rSCBF after irreversible ischemia are the direct reason of the protection of ischemic preconditioning to spinal cord neurofunction, which was proved by spinal cord evoked potentials (SCEP). Conclusions: 5 minutes ischemic preconditioning can increase the rSCBF, enhance the tolerance of the spinal cord to irreversible ischemia and definitely protect the neurofunction of the spinal cord. The biological mechanism of the protection of ischemic preconditioning to spinal cord ischemia should be further studied.