Brain O2 consumption and glutamate release during hypoglycémie coma in piglets are temperature sensitive

R. N. Ichord, F. J. Northington, D. Van Wylen, M. V. Johnston, C. Kwon, R. J. Traystman

Research output: Contribution to journalArticle

Abstract

Hypoglyce-mic injury in the mature brain is mediated by excitotoxicity, which is worsened by disordered cellular energy metabolism. The role of excitotoxicity in relation to brain energy metabolism during hypoglycemia has not been studied in the immature brain. Brain oxygen consumption (CMR0 ) increases during hypoglycemia in piglets, whereas CMR O2 decreases in adult pig models. We tested the hypothesis that increased CMR O2 during hypoglycémie coma is temperature dependent and coincides with increased excitatory amino acids (EAA). We measured cerebral blood flow (CBF), CMRO2, and cortical microdiaysate EAAin pentobarbital-anesthetized piglets during hypoglycémie coma and during 2 h of recovery and in normoglycemic controls. In warmed animals brain temperature was kept normothermic (38.5°C). In unwarmed animals brain temperature was allowed to fall (37.6°C). During hypoglycemia CBF increased similarly in warmed animals and unwarmed animals; CMR0 increased in warmed animals but not unwarmed animals. Glutamate increased during coma and increased more in warmed animals than unwarmed animals but normalized quickly during recovery. EEG recovered earlier in unwarmed animals. We conclude that during a hypoglycémie coma in the immature brain, CMRU2 and glutamate are increased in a temperature-dependent manner. newborn; cerebral blood flow; excitotoxicity; microdialysis; electroencephalogram

Original languageEnglish (US)
Pages (from-to)H2063-H2068
JournalAmerican Journal of Physiology
Volume276
Issue number6 PART 2
StatePublished - Dec 1 1999

ASJC Scopus subject areas

  • Physiology (medical)

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