Brain slices gain water when maintained in bicarbonate-buffered artificial
cerebro-spinal fluid (ACSF) at 35 degreesC. We previously showed that this
edema is linked to glutamate receptor activation and oxidative stress. An a
dditional factor that may contribute to swelling is acidosis, which arises
from high CO2 tension in brain slices. To examine the role of acidosis in s
lice edema, we added N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (H
EPES) to osmotically balanced ACSF (HEPES-ACSF), thereby increasing bufferi
ng capacity beyond that provided by bicarbonate/CO2. Water gain was markedl
y inhibited in HEPES-ACSF. After 3 h incubation in HEPES-ACSF at 35 degrees
C, water gain was limited to that of fresh slices after 1 h recovery in ACS
F at room temperature. The effect of HEPES in decreasing slice water gain w
as concentration dependent from 0.3 to 20 mM. The inhibition of water gain
by HEPES suggests that tissue acidosis is a contributing factor in brain sl
ice edema. (C) 2001 Published by Elsevier Science Ireland Ltd.