Brain ischemia is the leading pathopysiological mechanism in the development of secondary brain damage after
acute subdural hematoma (SDH).
Hypothermia has been employed as an effective cerebroprotective treatment on
brain injuries, but the control of the general condition is very difficult under
hypothermia, and various severe complications have been reported. Cerebral
acidosis in the ischemic area is one of the important factors augmenting the
brain edema formation.
Tris-(hydroxymethyl)-aminomethane (THAM) has been used as an alkalizing agent for
acidosis on
brain injury and is reported to be effective. In the present study, we used a rat acute SDH model to assess the effect of mild (35 degrees C)
hypothermia and THAM combined treatment on brain water content,
brain ischemia, and blood-brain barrier (BBB) permeability at 4 h after
hematoma induction. Mild
hypothermia did not significantly reduce the brain water content beneath the
hematoma (79.5 +/- 0.2%) compared to normothermia (80.2 +/- 0.2%), but mild
hypothermia combined to THAM resulted in a significant reduction (78.7 +/- 0.0%; p < 0.01). Combined with mild
hypothermia, THAM treatment significantly reduced the
Evan's blue extravasation (35 +/- 7 ng/g wet tissue; p < 0.05) compared to normothermia (63 +/- 7 ng/g wet tissue). Furthermore, the volume of
infarction at 24 h after the
hematoma induction (54 +/- 3 mm(3); p < 0.01) was significantly smaller by the combined treatment compared with normothermia (70 +/- 2 mm(3)). The present findings indicate that mild
hypothermia of 35 degrees C combined with THAM presents a potent cerebroprotective strategy. The protection of the BBB is one of the possible cerebroprotective mechanisms in this rat acute SDH model.