MECHANISMS OF VASCULAR INJURY AFTER SPINAL CORD TRAUMA

急性脊髓损伤的早期药物干预 基于这样的前提，即最初的侮辱后的二次伤害 会导致最终的脊髓损伤和神经功能缺陷。这 最近对第二个问题的观察加强了争论 国家急性脊髓损伤研究(NASCIS II)显示高 伤后8小时内给予甲基强的松龙可改善神经功能 急性脊髓损伤患者的康复情况。脊髓损伤后进行性血管损伤 会造成二次伤害。血管损伤是该病的一个显著特征 急性炎症。急性炎症的所有基本特征 包括急性炎症细胞的沉积，积聚 炎症介质、内皮损伤导致血管增加 损伤脊髓内可见通透性和水肿性形成。我们 将继续探讨继发性损伤的血管机制 关注创伤后炎症反应在慢性阻塞性肺疾病发病机制中的作用 进行性血管损伤。这项提案的主要主题将是 激肽原-激肽系统和二十烷类化合物。细胞的作用 与激动素-二十烷素级联相关的炎症体液因子 将对其进行深入研究，探讨其细胞和分子机制。 创伤后进行性血管损伤 炎症反应。新的治疗方案也将被设计出来 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.