Hyperbaric oxygen therapy for reduction of secondary brain damage in head injury: an animal model of brain contusion
Palzur E, Vlodavsky E, Mulla H, Arieli R, Feinsod M, Soustiel JF. 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. PMID: 14987464 [PubMed - indexed for MEDLINE]
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