中文摘要：

目的建立长期稳定的兔脊髓静脉高压模型，用于研究脊髓血管畸形致病机制。方法36只新西兰大白兔随机分为短期组、中期组和长期组，每组手术造模8只和假手术兔4只。手术组兔通过开腹侧侧吻合兔左肾动静脉，形成动静脉瘘，结扎后腔静脉远端和近端导致动脉血异常引流至腰静脉、椎管内静脉丛形成脊髓淤血和脊髓静脉高压。采用Jacobs法对后肢功能评级，Reuter法对脊髓感觉运动反射功能评分，连续观察行为学变化，每组动物到期后对脊髓行MRI扫描、经股动脉DSA检查动静脉瘘口的通畅，并解剖取脊髓行病理学检查。结果24只模型兔中，存活22只，生存率91．67％，动静脉瘘口通畅率95．45％。术后模型后肢的运动、感觉功能均有所减退，与对照组比较差异有统计学意义。脊髓MRI表现为脊髓相应阶段的水肿，但判断脊髓静脉高压早期病理改变缺乏特异性。组织病理学在光镜下见脊髓内毛细血管的扩张充血，随时间的不同呈现血管周围淋巴细胞的浸润、胶质细胞的增生、髓内血管的玻璃样变性和神经元细胞变性，符合脊髓静脉高压的脊髓病理变化。透射电镜观察可见髓鞘板层的松散、薄髓纤维内线粒体数目的增加和神经元的固缩。结论通过该方法建立模拟人类脊髓血管畸形的脊髓静脉高压机制导致脊髓损伤的动物模型；模型可靠性和稳定性较高。

英文摘要：

Objective To establish a stable model of spinal cord venous hypertension in rabbits. Methods Thirty-six rabbits were recruited and randomly divided into three groups：short-term, mid-half, long-term. In each group,8 rabbits were subjected to arteriovenous fistula establishment, and the rest 4 to sham operation, respectively. Side to side anastomosis between left renal artery and vein was performed to establish the arteriovenous fistulas. We ligated the distal end of the inferior vena cave as well as its proximal end, in order to make the arterial blood stream drains anomalously to lumbar veins and internal vertebral veins, resulting in spinal cord congestion and spinal cord venous hypertension. The grade of hind limb function was assayed with Jacobs method, and the kinetic and sensory function of spinal reflex were scored with Reuter method. The changes of behavior in rabbits were observed continuously. MRI and DSA from femoral artery were performed among rabbit models in each group on time to check the arteriovenous fistulas, and then the animals were sacrificed after perfusion and the spinal cord was removed for histopathologic examination. Results Of the 24 animals in model group,22 survived and 2 died. The survival rate was 91.67%. The kinetic and sensory function of hind limb was decreased after operation as compared with control groups. MRI showed the spinal cord edema at the corresponding stage, but which used for judgement of early pathologic change of spinal cord venous hypertension was not specific. Under light microscopy, the pathological features of spinal cord hypertension were marked capillary expansion and congestion within the spinal cord, perivascular lymphocyte infiltration, gliosis, hyalinized vessels in spinal cord, neurons cellular degeneration. Transmission electron microscopy revealed myelin sheath layers loose, the increased number of nfitochondria within thin-myelinated fibers, and pycnosis neurons. Conclusion We established an animal model of spinal cord injury caused by spinal cord ven