PMID- 14987464
OWN - NLM
STAT- MEDLINE
DCOM- 20040512
LR  - 20161124
IS  - 0897-7151 (Print)
IS  - 0897-7151 (Linking)
VI  - 21
IP  - 1
DP  - 2004 Jan
TI  - Hyperbaric oxygen therapy for reduction of secondary brain damage in head injury: 
      an animal model of brain contusion.
PG  - 41-8
AB  - Cerebral contusions are one the most frequent traumatic lesions and the most 
      common indication for secondary surgical decompression. The purpose of this study 
      was to investigate the physiology of perilesional secondary brain damage and 
      evaluate the value of hyperbaric oxygen therapy (HBOT) in the treatment of these 
      lesions. Five groups of five Sprague-Dawley rats each were submitted to dynamic 
      cortical deformation (DCD) induced by negative pressure applied to the cortex. 
      Cerebral lesions produced by DCD at the vacuum site proved to be reproducible. 
      The study protocol entailed the following: (1) DCD alone, (2) DCD and HBOT, (3) 
      DCD and post-operative hypoxia and HBOT, (4) DCD, post-operative hypoxia and 
      HBOT, and (5) DCD and normobaric hyperoxia. Animals were sacrificed after 4 days. 
      Histological sections showed localized gross tissue loss in the cortex at injury 
      site, along with hemorrhage. In all cases, the severity of secondary brain damage 
      was assessed by counting the number of terminal deoxynucleotidyl 
      transferase-mediated dUTP nick end labeling (TUNEL) and caspase 3-positive cells 
      in successive perilesional layers, each 0.5 mm thick. Perilesional TUNEL positive 
      cells suggested the involvement of apoptosis in group 1 (12.24% of positive cells 
      in layer 1). These findings were significantly enhanced by post-operative hypoxia 
      (31.75%, p < 0.001). HBOT significantly reduced the severity and extent of 
      secondary brain damage expressed by the number of TUNEL positive cells in each 
      layer and the volume of the lesion (4.7% and 9% of TUNEL positive cells in layer 
      1 in groups 2 and 4 respectively, p < 0.0001 and p < 0.003). Normobaric hyperoxia 
      also proved to be beneficial although in a lesser extent. This study demonstrates 
      that the vacuum model of brain injury is a reproducible model of cerebral 
      contusion. The current findings also suggest that HBOT may limit the growth of 
      cerebral contusions and justify further experimental studies.
FAU - Palzur, Eilam
AU  - Palzur E
AD  - Division of Neurosurgery and Acute Brain Research Laboratory, Rambam Medical 
      Center, Faculty of Medicine, The Technion, Haifa, Israel.
FAU - Vlodavsky, Eugene
AU  - Vlodavsky E
FAU - Mulla, Hani
AU  - Mulla H
FAU - Arieli, Ran
AU  - Arieli R
FAU - Feinsod, Moshe
AU  - Feinsod M
FAU - Soustiel, Jean F
AU  - Soustiel JF
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PL  - United States
TA  - J Neurotrauma
JT  - Journal of neurotrauma
JID - 8811626
RN  - EC 3.4.22.- (Casp3 protein, rat)
RN  - EC 3.4.22.- (Caspase 3)
RN  - EC 3.4.22.- (Caspases)
SB  - IM
MH  - Animals
MH  - Apoptosis/physiology
MH  - Brain/*pathology
MH  - Brain Injuries/*therapy
MH  - Caspase 3
MH  - Caspases/metabolism
MH  - Disease Models, Animal
MH  - *Hyperbaric Oxygenation
MH  - Hypoxia/pathology
MH  - Immunohistochemistry
MH  - In Situ Nick-End Labeling
MH  - Rats
MH  - Rats, Sprague-Dawley
EDAT- 2004/02/28 05:00
MHDA- 2004/05/13 05:00
CRDT- 2004/02/28 05:00
PHST- 2004/02/28 05:00 [pubmed]
PHST- 2004/05/13 05:00 [medline]
PHST- 2004/02/28 05:00 [entrez]
AID - 10.1089/089771504772695931 [doi]
PST - ppublish
SO  - J Neurotrauma. 2004 Jan;21(1):41-8. doi: 10.1089/089771504772695931.