Figure 7

Stress-dose hydrocortisone results in reduced blood–brain-barrier permeability in the hypothalamus. Representative photographs of the brains from the stress-dose hydrocortisone (HC) group (A) and injury control group (B) and following Evans Blue (EB) dye injection on post-injury day 3. Summary data present the EB extravasation (C) and brain water content (D) in the hypothalamus at 3, 7 and 14 days after injury. The water content of the hypothalamus was significantly decreased in the stress-dose HC-treated rats as compared to injury controls (analysis of variance (ANOVA), F_(4,31) = 5.474, P = 0.002; post hoc least significant difference test (LSD), P = 0.001 for stress-dose HC versus injury control), and significant reduction in EB extravasation was also observed in the injured rats treated with stress-dose HC at 3 days after traumatic brain injury (ANOVA, F_(4,31) = 9.729, P = 0.000; post hoc LSD, P = 0.002 for stress-dose HC versus injury control). At each time point: n = 3 from each of the two groups (naïve and HC normal), n = 10 from each of three groups (injury control, low-dose methylprednisolone (MP), and stress-dose HC). ^*P <0.05 as compared to naive; ^#P <0.05 as compared to injury control. Data were expressed as mean ± standard error of the mean.