MECHANISMS OF VASCULAR INJURY AFTER SPINAL CORD TRAUMA

急性脊髓损伤（SCI）的早期药物干预是 根据的前提是，在最初的侮辱之后的二次伤害 最终导致脊髓损伤和神经功能缺损。 这 第二次世界大战后， 国家急性脊髓损伤研究（NASCIS II）显示， 在损伤后8小时内给予甲基强的松龙，可改善神经功能 急性SCI患者的康复。脊髓损伤后进行性血管损伤 会造成二次伤害血管损伤是一个突出的特点， 急性炎症急性炎症的所有主要特征 包括急性炎症细胞的沉积， 炎症介质，内皮损伤导致血管 在损伤的脊髓中已经注意到渗透性和水肿形成。我们 将继续探讨血管继发性损伤的机制 着重探讨创伤后炎症反应在创伤性脑血管病发病机制中的作用 进行性血管损伤 本提案的主题将是 激肽原-激肽系统和类花生酸谱。 细胞的作用 与激肽-类花生酸级联反应相关的炎症体液因子 将深入研究，探讨细胞和分子机制， 创伤后进行性血管损伤 炎症反应。还将设计新的治疗方案 基于这些研究。

Early pharmacological intervention in acute spinal cord injury (SCI) is based on the premise that secondary injury following the initial insult contributes to ultimate spinal cord damage and neurologic deficit. This contention is strengthened by the recent observation of the Second National Acute Spinal Cord Injury Studies (NASCIS II) showing that high dose methylprednisolone given within 8 hours of injury improved neurologic recovery in patients with acute SCI. Progressive vascular injury after SCI contributes to secondary injury. Vascular injury is a prominent feature in acute inflammation. All the cardinal features of acute inflammation including deposition of acute inflammatory cells, accumulation of inflammatory mediators, endothelial damage leading to increased vascular permeability and edema formation have been noted in the injured cord. We will continue to explore the vascular mechanism of secondary injury focusing on post-traumatic inflammatory reaction in the pathogenesis of progressive vascular injury. The main theme of this proposal will be on the kininogen-kinin system and eicosanoid profile. The roles of cellular and humoral factors of inflammation relevant to kinin-eicosanoid cascade will be studied in depth to explore cellular and molecular mechanism of progressive vascular injury in the context of a post-traumatic inflammatory reaction. New therapeutic regimens will also be designed based on these studies.