• H M Bramlett, E J Green, and W D Dietrich.
• Department of Neurological Surgery, and Neurotrauma Research Center, University of Miami, Florida 33101, USA.
• J. Neurosurg. 1999 Oct 1; 91 (4): 653-9.

ObjectPatients with head injuries often experience respiratory distress that results in a secondary hypoxic insult. The present experiment was designed to assess the histopathological consequences of a secondary hypoxic insult by using an established rodent model of traumatic brain injury (TBI).MethodsIntubated anesthetized rats were subjected to moderate (1.94-2.18 atm) parasagittal fluid-percussion injury (FPI) to the brain. Following the TBI, the animals were maintained for 30 minutes by using either hypoxic (TBI-HY group, nine animals) or normoxic (TBI-NO, 10 animals) gas levels. Sham-operated animals also underwent all manipulations except for the FPI (sham-HY group, seven animals; and sham-NO group, seven animals). Three days after TBI the rats were killed, and quantitative histopathological evaluation was undertaken. Cortical contusion volumes were dramatically increased in the TBI-HY group compared with the TBI-NO group (p < 0.03). Qualitative assessment of cortical and subcortical structures demonstrated significant damage within the hippocampal areas, CA1 and CA2, of TBI-HY animals compared with the TBI-NO animals (both p < 0.03). There was also a significant increase in the frequency of damaged neuronal profiles within the middle and medial sectors of the CA1 hippocampus (p < 0.03) due to the hypoxic insult.ConclusionsThe results of this study demonstrate that a secondary hypoxic insult following parasagittal FPI exacerbates contusion and neuronal pathological conditions. These findings emphasize the need to control for secondary hypoxic insults after experimental and human head injury.

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