The effects of traumatic brain injury on cerebral blood flow and brain tissue nitric oxide levels and cytokine expression.

Adult, male, Sprague-Dawley rats were anesthetized, intubated, and mechanically ventilated with 1.5-2.0% isoflurane in oxygen (30%) and air. Rats were prepared for fluid percussion traumatic brain injury (TBI), laser Doppler flowmetry, and measurement of brain tissue nitric oxide (NO) levels using an ISO-NO electrode system. After preparation, isoflurane was reduced to 1.5%, and the rats were randomly assigned to receive sham (n = 6), moderate (1.9 atm, n = 6), or severe (2.8 atm, n = 6) parasagittal fluid percussion TBI. CBF and brain tissue NO levels were measured for 4 h, and then isoflurane levels were increased to 4.0% and the rats were decapitated and the brains were removed. Total RNA was isolated from rat brains and cytokine expression was determined. Laser Doppler flow velocity remained constant in the sham-injured rats but decreased significantly in rats subjected to moderate (p 0.05) or severe (p 0.05) TBI. Brain tissue NO levels remained constant in the sham-injured rats but decreased significantly (p 0.01) after moderate TBI. Severe TBI produced slight, insignificant reductions in NO levels. Cytokine expression was very low in the shaminjured rats. TBI-induced expression of mRNAs for interleukin-1 alpha (IL-1alpha), IL-1beta, IL-6, and tumor necrosis factor-alpha (TNFa). IL-1alpha and IL-1beta mRNA expression increased significantly (p 0.05 vs. sham-injury) after severe TBI and IL-6 and TNFa mRNA expression increased significant (p 0.05 vs. sham-injury) after both moderate and severe TBI. Other cytokine mRNA expression was unchanged after TBI.