Mj. Whalen et al., THE EFFECT OF BRAIN TEMPERATURE ON ACUTE-INFLAMMATION AFTER TRAUMATICBRAIN INJURY IN RATS, Journal of neurotrauma, 14(8), 1997, pp. 561-572
The effect of varying brain temperature on neutrophil accumulation in
brain and the expression of E-selectin and intercellular adhesion mole
cule-1 (ICAM-1) on cerebrovascular endothelium after controlled cortic
al impact (CCI) was studied in rats. Sprague Dawley rats were anesthet
ized and subjected to CCI to the left parietal cortex. Ten minutes aft
er CCI, brain temperature was modulated and maintained at 32 degrees C
, 37 degrees C, or 39 degrees C (n = 8 per group) for 4 h. Rats were t
hen decapitated and immunohistochemistry on brain sections was perform
ed using monoclonal antibodies (MoAb) that recognize neutrophils (RP-3
), ICAM-1 (TM-8, Athena Neurosciences), or MoAb that react with E-sele
ctin (La-Roche). Each of these markers was quantified in 100 x fields.
Neutrophil accumulation was also quantified with myeloperoxidase (MPO
) assay. Absolute neutrophil count (ANC) was measured in blood samples
before and 1 h and 4 h after CCI. Neutrophil accumulation in injured
brain was decreased in rats maintained at 32 degrees C vs 39 degrees C
(4-fold difference as assessed by immunohistochemistry, p < 0.05; 8-f
old difference as assessed by MPO assay, p < 0.05). Peripheral blood A
NC was not affected by temperature. E-selectin was induced on cerebrov
ascular endothelium after CCI (p < 0.05), but was only decreased modes
tly at 32 degrees C versus 39 degrees C (p = 0.11). ICAM-1 was not upr
egulated on cerebrovascular endothelium at this early time following C
CI. Neutrophil accumulation is directly dependent on brain temperature
during the initial 4 h after CCI. This appears to be mediated by mech
anisms other than effects of temperature on E-selectin or ICAM-1 expre
ssion or systemic ANC.