LONG-TERM EXPOSURE TO HEAT REDUCES EDEMA FORMATION AFTER CLOSED-HEAD INJURY IN THE RAT

Cerebral edema is one of the major consequences of head trauma (HT); i ts evolution may cause secondary ischemia and neuronal damage. In a cl osed head injury model in rats, we have shown BBB disruption and edema formation during the post traumatic period. We have previously shown that chronic exposure to moderate heat improves clinical outcome of ra ts subjected to HT. Long term exposure to heat results in the achievem ent of a stable acclimated state, characterized by a lower metabolic r ate and improved heat tolerance. In the present study, we investigated the effect of chronic exposure to heat on edema formation after HT. R ats were held at 24-degrees-C (CON) or 34-degrees-C (ACC) for one mont h. Injury was then induced under ether anesthesia by a weight drop dev ice. Four or 48 hours later, they were sacrificed for evaluation of BB B integrity (Evans blue, EB, extravasation) or edema formation (specif ic gravity, SG, or percent water). We found that EB uptake by the cont used hemisphere was 6 fold lower in the ACC rats as compared to CON (p < 0.001). Furthermore, edema measured at 48 h by both SG and percent water methods was significantly lower in the acclimated rats (p < 0.01 ). We suggest that heat acclimation offers protection to rats subjecte d to head injury, possibly by reduction of plasma proteins extravasati on.