大鼠慢性压迫性颈脊髓症神经血管单元的超微结构

Ultrastructure of neurovascular unit in chronic compressive cervical myelopathy rat model

目的观察慢性颈脊髓压迫sD大鼠模型不同时段神经血管单元（NVU）超微结构变化特征。方法2014年3月至2015年3月，将32只SD大鼠随机分为对照组和实验组。后者制作慢性颈脊髓压迫模型后，运用BBB评分及体感诱发电位（SEP）评价造模大鼠的脊髓神经功能，并分别于造模后第14、21、28、42天处死动物取样制作电镜样本，用透射电镜观察受压部位灰质NVU超微结构变化。结果造模后实验组第14、21、28和42天BBB评分分别为17．571±0．870、15．952±0．870、15．476±0．602和16．190±0．750，均显著低于对照组（4个时间点分别为19．600±0．516、19．500±0．527、19．600±0．699和19．800±0．632）．差异有统计学意义（P〈0．05）；实验组SEP的潜伏期比对照组明显延长、波幅显著降低（P〈0．05）；电镜提示早期（第14～28天）内皮细胞、基膜破坏，线粒体、星形胶质细胞水肿，轴索排列紊乱；后期（第42天）内皮细胞和基膜呈代偿和修复改变，星形胶质细胞，线粒体恢复正常，但是轴索修复不完全。结论慢性压迫性颈脊髓损伤早期（第14～21天）神经血管单元出现破坏，6周后会得到一定程度修复，但修复不完全。

Objective To observe the uhrastructure of the neurovascular Unit （NVU） in chronic compressive cervical myelopathy rat model at different stages. Methods From March, 2014 to March, 2015, 32 rats were di- vided into two groups： sham control group （n = 8） and compressive spinal cord injury group （n = 24）. The model was established by inserting the compression sheet made of polyurethane at the level of C6. BBB and somatosensory evoked potentials （SEP） were used to evaluate the spinal cord function status of model rat. Transmission Electron Microscopy （TEM） examination of compressive cervical spinal cords was performed separately at the 14th, 21st, 28th and 42nd day after modeling. Results At the 14th, 21st, 28th and 42nd, the BBB score were 17.571 ± 0.870, 15.952± 0.870, 15.476 ± 0.602 and 16.190 ± 0.632 were significantly lower than those in the control group （the BBB score of 4 points were 19.600 ± 0.516, 19.500 ±0.527, 19.600 ± 0.699 and 19.800 ± 0.6232 respectively） （P 〈 0.05）. Latency prolon- gation and amplitude reduction of somatosensory evoked potentials （SELP） were presented in the compressive spinal cord injury group. At the 14th day, edema around the capillaries was observed, the morphological structure of endothelial cells and basement membrane was normal, the tight junction between endothelial cell was intact, the mito- chondria in the axons, oligodendrocytes and astrocyte foot processes were edematous. At the 21st day, extensive ede- ma, even partial necrosis around the capillaries were found, the surrounding structure were arranged loosely, partial loss of endothelial cells and basement membrane, cavitation occurrence in endothelial cells, basal membrane density was significantly lower, mitochondria vacuoles and shrinkage in the cytoplasm, axon myelin loose or broken; at the 28th day, the edematous range surrounding capillaries narrowed, low density of basement membrane and endothelial cells, vacuoles in endothelial cells, loose axon myelin, while some mitochondrias backed to normal. At the 42nd day, capillary integrity, no abnormalities were found in endothelial cells, basement membrane, tight junction and mito- chondria, double layers of endothelial cells and basement membrane could be seen, local broken and loose structure were presented in part of the axons; The TEM of the sham control group showed normal ultrastructure of NVU. Conclusion The uhrastructure of NVU in chronic cervical spinal cord compression presented various in the different periods, NVU disruption were found in the early stages （14th-28th days）, and compensatory and repair process were developed incompletely later.