PMID- 14753503
OWN - NLM
STAT- MEDLINE
DCOM- 20040309
LR  - 20190917
IS  - 0065-1419 (Print)
IS  - 0065-1419 (Linking)
VI  - 86
DP  - 2003
TI  - Metabolic derangements in interstitial brain edema with preserved blood flow: 
      selective vulnerability of the hippocampal CA3 region in rat hydrocephalus.
PG  - 545-7
AB  - Hydrocephalus induces interstitial brain edema, which causes neurological 
      deficits, even if the intracranial pressure is maintained within the normal 
      range, and the cerebral blood flow (CBF) does not decline to an ischemic level. 
      The precise mechanisms underlying such edema-induced neuronal dysfunction remain 
      unclear. In the present study, in an attempt to elucidate the metabolic 
      derangements in brain tissue with interstitial edema, we evaluated the changes in 
      CBF and oxidative/glucose metabolism using a rat model of kaolin-induced 
      hydrocephalus. Hydrocephalus was produced in male Wistar rats by intrathecal 
      injection of 0.1 ml aluminum silicate suspension (200 mg/ml) via the cisterna 
      magna. CBF was determined by 14[C]-iodoantipyrine autoradiography. Oxidative 
      metabolism was evaluated by cytochrome oxidase (CYO) histochemistry, and glucose 
      metabolism by hexokinase (HK) histochemistry. CBF declined with the development 
      of hydrocephalus, but did not reach an ischemic level. The CYO activity was 
      diffusely depressed in both the cortex and hippocampus. The HK activity was 
      preserved at the early stage of hydrocephalus. At the advanced stage, the HK 
      activity was reduced in the hippocampal CA3 region first, and diffusely 
      thereafter. In conclusion, interstitial brain edema impairs oxidative metabolism 
      even at the early stage of hydrocephalus, and shifts the metabolism to anaerobic 
      glycolysis despite a preserved CBF. Impairment of glucose metabolism was first 
      observed in the CA3 region, suggesting that the CA3 is metabolically vulnerable, 
      and CA3 dysfunction may contribute to the memory deficits seen in hydrocephalus.
FAU - Kawamata, T
AU  - Kawamata T
AD  - Department of Neurological Surgery, Nihon University School of Medicine, Tokyo, 
      Japan. kawamata@med.nihon-u.ac.jp
FAU - Katayama, Y
AU  - Katayama Y
FAU - Tsuji, N
AU  - Tsuji N
FAU - Nishimoto, H
AU  - Nishimoto H
LA  - eng
PT  - Journal Article
PL  - Austria
TA  - Acta Neurochir Suppl
JT  - Acta neurochirurgica. Supplement
JID - 100962752
RN  - EC 1.9.3.1 (Electron Transport Complex IV)
RN  - EC 2.7.1.1 (Hexokinase)
SB  - IM
MH  - Animals
MH  - Autoradiography
MH  - Body Water/metabolism
MH  - Brain/*metabolism
MH  - Brain Edema/metabolism/*physiopathology
MH  - *Cerebrovascular Circulation
MH  - Electron Transport Complex IV/metabolism
MH  - Hexokinase/metabolism
MH  - Hippocampus/*physiopathology
MH  - Hydrocephalus/*physiopathology
MH  - Rats
MH  - Rats, Wistar
EDAT- 2004/02/03 05:00
MHDA- 2004/03/10 05:00
CRDT- 2004/02/03 05:00
PHST- 2004/02/03 05:00 [pubmed]
PHST- 2004/03/10 05:00 [medline]
PHST- 2004/02/03 05:00 [entrez]
AID - 10.1007/978-3-7091-0651-8_111 [doi]
PST - ppublish
SO  - Acta Neurochir Suppl. 2003;86:545-7. doi: 10.1007/978-3-7091-0651-8_111.