脊髓損傷會造成神經組織內的血管破損，進而導致許多發炎細胞從這些破碎的血管內滲出，進一步擴大損傷的範圍。因此，完整的血管結構對於脊髓損傷後的組織修復相當重要。正常的脊髓組織中，血管的外圍含有血－脊髓障壁（blood-spinal cord barrier）的結構，其組成包括了內皮細胞、基底膜以及星狀膠細胞。本實驗以免疫螢光染色法研究脊髓損傷後第1,3,7,14,21以及28天新生血管的分佈以及結構型態。脊髓損傷後新生血管的形態常常是不規則的，它們管徑擴大且呈現彎曲。本研究發現存在於損傷中心的新生血管大部分並沒有星狀膠細胞的貼附。基底膜內的細胞外基質包含膠原蛋白（Collagen type IV）與粘連蛋白（Laminin），損傷後第7天這兩種細胞外基質蛋白從損傷中心蔓延開來並持續到第28天。此外，纖維粘連蛋白（Fibronectin）也在損傷之後大量表現，新生的血管都分佈在這些細胞外基質所形成的絲狀結構之中。使用luxol fast blue染色法觀察受損脊髓內髓鞘磷脂分佈的面積並評估運動行為復原的結果後發現血管新生與運動功能的回復並沒有太大的關聯性。

After spinal cord injury, the blood vessels in the cord are disrupted, leading to the infiltration of inflammatory cells which further damage the tissue. Thus re-establishing the blood vessels is important to restore nutrition and oxygen supplies that facilitate neuronal regeneration and functional recovery after spinal cord injury. Normally, astrocytes and several extra-cellular matrix (ECM) components including laminin and collagens are integral to the vascular barrier. After spinal cord injury, however, the relationship among astrocytes, ECM, and newly-formed blood vessels has not been completely examined. I found that the newly-formed blood vessels exhibited dilated and fragmental morphology with a defective vascular barrier for lack of perivascular astrocytes 7 to 28 days post-injury. Both laminin and collagen not only surrounded those newly-formed blood vessels, as observed in uninjured vessels, but also substantially spread among vessels from 7 to 28 days post-injury. Furthermore, fibronectin, which plays an important role during wound healing but does not exist around normal vessels in the uninjured spinal cord, appeared outside the newly-formed vessels in the lesion at 1 day post-injury, became apparent at 3 days post-injury, and spread all over the lesion from 7 days post-injury afterwards. The size of residual white matter stained by luxol fast blue and the improvement in motor function were not associated with the vascular density in the lesion. My results show that the newly-formed blood vessels in the injured spinal cord have defective structure and changed morphology with significantly increased ECM expression between the vessels.

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