Superoxide and Nitric Oxide Mechanisms in Traumatic Brain Injury and Hemorrhagic Hypotension.
Abstract
Traumatic brain injury (TB I) reduces cerebral blood flow (CBF) and renders the brain vulnerable to secondary ischemia. Hypotension contributes to poor Outcome after TBI in humans. We have prevented hypoperfusion and restored autoregulation after TBI. The goals of this project are to determine whether treatment based on our observations will prevent CBF reductions, brain edema and histological damage after TBI and hemorrhagic hypotension and to understand the mechanisms that contribute to the efficacy of the proposed treatments. Specific Aim 1 addressed the hypothesis that impairment of cerebrovascular function will result in brain injury after TBI and hemorrhagic hypotension that would not occur after hypotension alone. Specific Aim 2 addressed the hypothesis that post-TB I cerebral hypoperfusion is caused by nitric oxide (N0)-dependent mechanisms. Specific Aim 3 addressed the hypothesis that increased production of superoxide during TBI and subsequent hypotension/resuscitation is responsible for the impaired cerebrovascular reactivity. Specific Aim 4 will address the hypothesis that small volume resuscitation with hypertonic saline will restore cerebral circulatory and systemic hemodynamics without causing the pronounced changes in brain water diffusion seen after TBI and hypotension/resuscitation with shed blood.
Document Details
- Document Type
- Technical Report
- Publication Date
- Dec 01, 1998
- Accession Number
- ADA364962
Entities
People
- Douglas S. Dewitt
Organizations
- University of Texas Medical Branch