PMID- 9498846
OWN - NLM
STAT- MEDLINE
DCOM- 19980326
LR  - 20061115
IS  - 0271-678X (Print)
IS  - 0271-678X (Linking)
VI  - 18
IP  - 3
DP  - 1998 Mar
TI  - Mitochondrial function and energy metabolism after hypoxia-ischemia in the 
      immature rat brain: involvement of NMDA-receptors.
PG  - 297-304
AB  - Treatment after hypoxia-ischemia (HI) in immature rats with the 
      N-methyl-D-aspartate receptor (NMDAR) antagonist dizocilpine maleate (MK-801) 
      reduces areas with high glucose utilization and reduces brain damage. The object 
      was to study the metabolic effects of MK-801 treatment after HI. Seven-day-old 
      rats were randomized to the following groups: non-HI, HI, or HI plus MK-801 (0.5 
      mg/kg immediately after HI). In the parietal cortex, the mitochondrial 
      respiration was measured in homogenates 1 to 4 hours, and the energy metabolites 
      at 3 and 8 hours after HI. The energy use was calculated from changes in energy 
      metabolites after decapitation at 3 hours after HI. State 3 respiration was 
      reduced by 46%, 32%, and 25% after HI compared with non-HI with pyruvate plus 
      malate, glutamate plus malate, or glutamate plus succinate as substrates, 
      respectively. Uncoupler-stimulated but not state 4 respiration was similarly 
      reduced. The MK-801 augmented pyruvate plus malate-supported state 3 respiration 
      after HI by 42%. The energy utilization was not affected by HI but was reduced by 
      MK-801 treatment in the ipsilateral cortex from 4.6 +/- 2.3 to 2.6 +/- 1.8 
      micromol high-energy phosphate bond/min/g. The levels of ATP and phosphocreatine 
      did not differ between the HI and HI plus MK-801 groups at 3 hours, but were 
      lower in the HI than in the HI plus MK-801 group at 8 hours after HI. In 
      conclusion, treatment with MK-801 reduced energy utilization and improved 
      mitochondrial function and energy status after HI, suggesting a linkage between 
      NMDAR activation and impaired energy metabolism during reperfusion.
FAU - Gilland, E
AU  - Gilland E
AD  - Department of Obstetrics and Gynecology, Goteberg University, Sweden.
FAU - Puka-Sundvall, M
AU  - Puka-Sundvall M
FAU - Hillered, L
AU  - Hillered L
FAU - Hagberg, H
AU  - Hagberg H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Cereb Blood Flow Metab
JT  - Journal of cerebral blood flow and metabolism : official journal of the 
      International Society of Cerebral Blood Flow and Metabolism
JID - 8112566
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
SB  - IM
MH  - Animals
MH  - Brain/*blood supply/growth & development/*metabolism/ultrastructure
MH  - Brain Ischemia/*metabolism/pathology
MH  - *Energy Metabolism
MH  - Mitochondria/*metabolism/pathology
MH  - Rats
MH  - Rats, Wistar
MH  - Receptors, N-Methyl-D-Aspartate/*metabolism
EDAT- 1998/03/14 00:00
MHDA- 1998/03/14 00:01
CRDT- 1998/03/14 00:00
PHST- 1998/03/14 00:00 [pubmed]
PHST- 1998/03/14 00:01 [medline]
PHST- 1998/03/14 00:00 [entrez]
AID - 10.1097/00004647-199803000-00008 [doi]
PST - ppublish
SO  - J Cereb Blood Flow Metab. 1998 Mar;18(3):297-304. doi: 
      10.1097/00004647-199803000-00008.