Accession Number : ADA337483
Title : Superoxide and Nitric Oxide Mechanisms in Traumatic Brain Injury and Hemorrhagic Hypotension.
Descriptive Note : Annual rept. 1 Dec 96-30 Nov 97
Corporate Author : TEXAS UNIV MEDICAL BRANCH AT GALVESTON
Personal Author(s) : DeWitt, Douglas S.
PDF Url : ADA337483
Report Date : DEC 1997
Pagination or Media Count : 75
Abstract : Traumatic brain injury (TBI) 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-TBI cerebral hypoperfusion is caused by nitric oxide (NO)-dependent mechanisms. Specific Aim 3 addressed the hypothesis that increased production of super oxide 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 hyper tonic 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.
Descriptors : *NITROGEN OXIDES, *TRAUMA, *BLOOD CIRCULATION, *CEREBROVASCULAR SYSTEM, *HYPOTENSION, *SUPEROXIDES, PRODUCTION, DAMAGE, BRAIN, HUMANS, WATER, SECONDARY, REACTIVITIES, WOUNDS AND INJURIES, DIFFUSION, HYPOTHESES, CIRCULATION, BLOOD, HISTOLOGY, RESUSCITATION, CEREBRUM, ISCHEMIA, HEMORRHAGE, EDEMA.
Subject Categories : Biochemistry
Anatomy and Physiology
Medicine and Medical Research
Distribution Statement : APPROVED FOR PUBLIC RELEASE