The role of glucose in brain injury following the combination of lipopolysaccharide or lipoteichoic acid and hypoxia-ischemia in neonatal rats.

Abstract:

:We have previously shown that lipopolysaccharide (LPS) sensitizes the immature rat brain to subsequent hypoxic-ischemic (HI) injury; however, the underlying mechanisms remain unclear. In this study, we examined the role of glucose in the sensitizing effects of LPS and lipoteichoic acid (LTA) in combination with HI in 7-day-old rats. LPS/HI resulted in hypoglycemia which lasted 24 h and lactate levels were increased from 6 to 10 h after LPS administration. LPS/HI induced severe brain injury, which persisted 2 weeks after LPS/HI. Administration of glucose to LPS-treated animals with HI reduced brain injury in the cerebral cortex and hippocampus, while striatal damage remained. LTA/HI did not affect blood glucose, lactate or brain injury. In conclusion, enhanced blood glucose levels during HI after LPS administration conferred protection in some brain regions but not in the striatum, suggesting that alterations in glucose can only partly explain the sensitizing effect of LPS.

journal_name

Dev Neurosci

authors

Eklind S,Arvidsson P,Hagberg H,Mallard C

doi

10.1159/000080713

keywords:

subject

Has Abstract

pub_date

2004-01-01 00:00:00

pages

61-7

issue

1

eissn

0378-5866

issn

1421-9859

pii

80713

journal_volume

26

pub_type

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