伴有脊髓损伤先天性脊柱侧凸实验模型的稳定性评估

Stability of a geneogenous scoliosis experimental model accompanied with spinal cord injury

背景：稳定、有效的先天性脊柱侧弯实验动物模型的建点是深入研究脊拄侧弯继发脊髓损伤的前提和研究分析脊髓损伤机制的有效路径。目的：评估伴有复杂脊髓损伤的先天性脊梓侧弯大白鼠动物模型的稳定性。方法：15只无明显脊髓神经症状的模型大白鼠被置入直径6cm的专用玻璃管中直立状态生活6-10d，建立脊能损伤合并先人性脊柱侧弯大鼠模型。结果与结论：13只大鼠均表现为双侧后肢瘫，后肢及尾部无活动，对针刺亦无反应，排尿障碍，排便未见明盟障碍：所有大鼠都出现烈侧后肢及尾部的皮毛枯萎，无光泽，部分开始脱毛。BBB评分平均为7．3-2．2。改良Tarlov评分：0级5只；1级2只；2级4只；3级1只；4级1只；5级0只。影像学观察示：先天性的缺陷遍布脊柱的所育节段；谯部分实验动物身上，还发现任侧弯顶点的楔形半椎体和间斑一起向椎管方向移位。组织化学观察示：骨与脊髓滋养血管破坏的先天性缺陷，与脊柱的骨性结构破坏部分对脊髓相应节段造成的压迫足一对应的；畸形顶点水甲，可见【血管分布缺失区域，存侧弯顶点水平脊柱静脉丛血管组织的凋亡现象。提示动物模型伴随的复杂脊髓损伤症状与先天性脊柱侧弯患儿临床病状的发腱过程奉鞘近似，动物模型的可重复率在87％（13／15）。

BACKGROUND： Establishment of a stable and effetive experimental animal model with congenital scoliosis is a precondition to lucubrate the congenital scotiosis with spinal cord injury and an efficient path to analyze the mechanism of spinal cord injury. OBJECTIVE： To assess the stability of congenital scoliosis model accompanied with complex spinal cord injury in rats. METHODS： A number of 15 model rats with no obvious spinal cord symptoms were put into special glass tubes with a diameter of 6 centimeters. The rats were kept in upright position in the tubes for 6 to 10 days to establish the congenital scoliosis model accompanied with complex spinal cord injury. RESULTS AND CONCLUSION： A total of 13 rats showed bilateral hind limb paralysis, adiaphoria of hind limbs and tail and no response to acupuncture and urination disorder. There were no obvious obstacles of defecation. The fur of bilateral hind limbs and tail in all the rats started to wither, became dull or even dropped. The mean Basso, Beattie and Bresnahen score was 7.3＋_2.2 Modified Tarlov scores were as follows, 0, 5 rats; 1,2 rats; 2, 4 rats; 3, 1 rat; 4, 1 rat; 5, 0 rat. According to imaging, the congenital scoliosis were all over the spinal cord. The wedged hemivertebra and intercalated disc at the scoliosis vertex moved towards the spinal canal in some rats. According to histochemical results, there was a one-to-one relationship between the congenital defect with bone-and-spinal nourishing vessels damage and the compression in spinal cord segments caused by the bone structure damage in the corresponding segments. There were visible vascular distribution deletion regions at the malformation vertex. The vascular tissue of the venoux plexus underwent apoptosis at the scoliosis vertex. These findings indicate that the symptoms of complex spinal cord injury accompanied with the congenital scoliosis model are similar to the symptoms progress of congenital scoliosis patients. The repeat rate of the rat model is 87% （13/15）.