Abstract

In this project we seek to elucidate the mechanisms responsible for the low CBF or ischemia found in the period immediately following severe head injury in man. We hypothesize that ischemia occurs despite adequate cerebral perfusion pressure and is not due to vasospasm of the larger, conducting vessels or too vigorous hyperventilation. As early as possible after injury, we will measure CBF, cerebral blood volume (CBV), AVDO1, AVD lactate, ICP and blood velocity with TECD, and, where clinically indicated, we will perform histological analysis of the brain microcirculation removed at surgery. Moreover, by combining the above data and data from continuous CBF (thermal dilution) and SjvO2 measurements with those from Project 1, we will support that project, and by combining CBV measurements and brain water mapping we will support Project 3.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Specialized Center (P50)
Project #
5P50NS012587-20
Application #
3738194
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
20
Fiscal Year
1995
Total Cost
Indirect Cost

  Institution

Name
Virginia Commonwealth University
Department
Type
DUNS #
City
Richmond
State
VA
Country
United States
Zip Code
23298

  Publications

Kleindienst, Andrea; Dunbar, Jana G; Glisson, Renee et al. (2013) The role of vasopressin V1A receptors in cytotoxic brain edema formation following brain injury. Acta Neurochir (Wien) 155:151-64
Brophy, Gretchen M; Mazzeo, Anna Teresa; Brar, Satjit et al. (2013) Exposure of cyclosporin A in whole blood, cerebral spinal fluid, and brain extracellular fluid dialysate in adults with traumatic brain injury. J Neurotrauma 30:1484-9
Prieto, Ruth; Tavazzi, Barbara; Taya, Keisuke et al. (2011) Brain energy depletion in a rodent model of diffuse traumatic brain injury is not prevented with administration of sodium lactate. Brain Res 1404:39-49
Fazzina, Giovanna; Amorini, Angela M; Marmarou, Christina R et al. (2010) The protein kinase C activator phorbol myristate acetate decreases brain edema by aquaporin 4 downregulation after middle cerebral artery occlusion in the rat. J Neurotrauma 27:453-61
Mazzeo, Anna Teresa; Brophy, Gretchen M; Gilman, Charlotte B et al. (2009) Safety and tolerability of cyclosporin a in severe traumatic brain injury patients: results from a prospective randomized trial. J Neurotrauma 26:2195-206
Fabricius, Martin; Fuhr, Susanne; Willumsen, Lisette et al. (2008) Association of seizures with cortical spreading depression and peri-infarct depolarisations in the acutely injured human brain. Clin Neurophysiol 119:1973-84
Mazzeo, Anna Teresa; Alves, Oscar Luis; Gilman, Charlotte B et al. (2008) Brain metabolic and hemodynamic effects of cyclosporin A after human severe traumatic brain injury: a microdialysis study. Acta Neurochir (Wien) 150:1019-31;discussion 1031
Lu, J; Marmarou, A; Choi, S et al. (2005) Mortality from traumatic brain injury. Acta Neurochir Suppl 95:281-5
Tavazzi, Barbara; Signoretti, Stefano; Lazzarino, Giuseppe et al. (2005) Cerebral oxidative stress and depression of energy metabolism correlate with severity of diffuse brain injury in rats. Neurosurgery 56:582-9; discussion 582-9
Signoretti, Stefano; Marmarou, Anthony; Tavazzi, Barbara et al. (2004) The protective effect of cyclosporin A upon N-acetylaspartate and mitochondrial dysfunction following experimental diffuse traumatic brain injury. J Neurotrauma 21:1154-67

Showing the most recent 10 out of 12 publications