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Am J Physiol Heart Circ Physiol 276: H2053-H2062, 1999;
0363-6135/99 $5.00
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Vol. 276, Issue 6, H2053-H2062, June 1999

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

R. N. Ichord1, F. J. Northington2, D. van Wylen5, M. V. Johnston4, C. Kwon4, and R. J. Traystman3

1 Departments of Neurology, 2 Pediatrics, and 3 Anesthesiology and Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, 21287; 4 Kennedy Krieger Institute, Baltimore, Maryland 21205; and 5 Department of Biology, St. Olaf College, Northfield, Minnesota 55057

Hypoglycemic 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 (CMRO2) increases during hypoglycemia in piglets, whereas CMRO2 decreases in adult pig models. We tested the hypothesis that increased CMRO2 during hypoglycemic coma is temperature dependent and coincides with increased excitatory amino acids (EAA). We measured cerebral blood flow (CBF), CMRO2, and cortical microdiaysate EAA in pentobarbital-anesthetized piglets during hypoglycemic 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; CMRO2 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 hypoglycemic coma in the immature brain, CMRO2 and glutamate are increased in a temperature-dependent manner.

newborn; cerebral blood flow; excitotoxicity; microdialysis; electroencephalogram


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