MECHANISMS OF VASCULAR INJURY AFTER SPINAL CORD TRAUMA

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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.