title: A new method for modulating traumatic brain injury with mechanical tissue resuscitation.
abstract: BACKGROUND
  Traumatic brain injuries remain a treatment enigma with devastating late results. As terminally differentiated tissue, the brain retains little capacity to regenerate, making early attempts to preserve brain cells after brain injury essential.
  
  
  OBJECTIVE
  To resuscitate damaged tissue by modulating edema, soluble cytokines, and metabolic products in the "halo" of damaged tissue around the area of central injury that progressively becomes compromised. By re-equilibrating the zone of injury milieu, it is postulated neurons in this area will survive and function.
  
  
  METHODS
  Mechanical tissue resuscitation used localized, controlled, subatmospheric pressure directly to the area of controlled cortical impact injury and was compared with untreated injured controls and with sham surgery in a rat model. Functional outcome, T2 magnetic resonance imaging hyperintense volume, magnetic resonance imaging spectroscopy metabolite measurement, tissue water content, injury cavity area, and cortical volume were compared.
  
  
  RESULTS
  There were significant differences between mechanical tissue resuscitation treated and untreated groups in levels of myoinositol, N-acetylaspartate, and creatine. Treated animals had significantly less tissue swelling and density than the untreated animals. Nonviable brain tissue areas were smaller in treated animals than in untreated animals. Treated animals performed better than untreated animals in functional tests. Histological analysis showed the remaining viable ipsilateral cerebral area was 58% greater for treated animals than for untreated animals, and the cavity for treated animals was 95% smaller than for untreated animals 1 month after injury.
  
  
  CONCLUSIONS
  Mechanical tissue resuscitation with controlled subatmospheric pressure can significantly modulate levels of excitatory amino acids and lactate in traumatic brain injury, decrease the water content and volume of injured brain, improve neuronal survival, and speed functional recovery.
authors.affiliation: Department of Plastic and Reconstructive Surgery, Wake Forest University Health Science, Winston-Salem, North Carolina 27157-1075, USA. largenta@wfubmc.edu
authors.forename: Louis C
authors.initials: LC
authors.lastname: Argenta
authors.forename: Zhenlin
authors.initials: Z
authors.lastname: Zheng
authors.forename: Allyson
authors.initials: A
authors.lastname: Bryant
authors.forename: Stephen B
authors.initials: SB
authors.lastname: Tatter
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Morykwas
mesh_terms: D000818:Animals; D001929:Brain Edema / Q000175:diagnosis* / Q000209:etiology / Q000517:prevention & control*; D001930:Brain Injuries / Q000150:complications / Q000175:diagnosis* / Q000534:rehabilitation*; D008297:Male; D054843:Negative-Pressure Wound Therapy / Q000379:methods*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012151:Resuscitation / Q000379:methods*; D016896:Treatment Outcome