• Naoki Aoyama, Stefan M Lee, Nobuhiro Moro, David A Hovda, and Richard L Sutton.
• UCLA Brain Injury Research Center, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, CA 90095-7039, USA.
• Brain Res. 2008 Sep 16; 1230: 310-9.

AbstractSecondary ischemia (SI) following traumatic brain injury (TBI) increases damage to the brain in both animals and humans. The current study determined if SI after TBI alters the extent or duration of reduced energy production within the first 24 h post-injury and hippocampal cell loss at one week post-injury. Adult male rats were subjected to sham injury, lateral (LFPI) or central fluid percussion injury (CFPI) only, or to combined LFPI or CFPI with SI. The SI was 8 min of bilateral forebrain ischemia combined with hemorrhagic hypotension, applied at 1 h following FPI. After LFPI alone adenosine triphosphate (ATP) levels within the ipsilateral CA1 were reduced at 2 h (p < 0.05) and subsequently recovered. After LFPI+SI the ATP reductions in CA1 ipsilateral to FPI persisted for 24 h (p < 0.01). ATP levels in the contralateral CA1 were not affected by LFPI alone or LFPI+SI. After CFPI alone CA1 ATP levels were depressed bilaterally only at 2 h (p < 0.05). Similar to the LFPI paradigm, CFPI+SI reduced ATP levels for 24 h (p < 0.01), with bilateral ATP reductions seen after CFPI+SI. Cell counts in the CA1 region at 7 days post-injury revealed no significant neuronal cell loss after LFPI or CFPI alone. Significant neuronal cell loss was present only within the ipsilateral (p < 0.001) CA1 after LFPI+SI, but cell loss was bilateral (p < 0.001) after CFPI+SI. Thus, SI prolongs ATP reductions induced by LFPI and CFPI within the CA1 region and this SI-induced energy reduction appears to adversely affect regional neuronal viability.

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