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Brain O2 consumption and glutamate release during hypoglycemic coma in piglets are temperature sensitive
R N Ichord1, F J Northington, D van Wylen
1Departments of Neurology, Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA. richord@jhmi.edu
The American Journal of Physiology
|June 11, 1999
Summary
Hypoglycemia causes brain injury in piglets, with increased brain oxygen consumption and glutamate levels that are temperature-dependent. Lowering brain temperature during hypoglycemia may protect the immature brain.
Area of Science:
- Neuroscience
- Pediatric Research
- Metabolic Disorders
Background:
- Hypoglycemic injury in the mature brain involves excitotoxicity and impaired energy metabolism.
- The impact of hypoglycemia on excitotoxicity and brain energy metabolism in immature brains remains understudied.
- Immature brains exhibit distinct responses to hypoglycemia, with increased cerebral oxygen consumption (CMRO2) unlike adult models.
Purpose of the Study:
- To investigate the temperature dependency of cerebral oxygen consumption (CMRO2) and excitatory amino acid (EAA) levels during hypoglycemic coma in immature brains.
- To test the hypothesis that increased CMRO2 during hypoglycemia in piglets is temperature-dependent and linked to elevated EAA.
- To compare the effects of normothermic versus hypothermic conditions on brain metabolism and neuronal injury markers during hypoglycemia.
Main Methods:
- Utilized pentobarbital-anesthetized piglets, divided into normothermic (warmed) and hypothermic (unwarmed) groups during induced hypoglycemic coma.
- Measured cerebral blood flow (CBF), cerebral oxygen consumption (CMRO2), and cortical microdialysate excitatory amino acids (EAA), including glutamate.
- Monitored electroencephalogram (EEG) recovery and brain temperature throughout the hypoglycemic coma and subsequent recovery period.
Main Results:
- Cerebral blood flow (CBF) increased similarly in both warmed and unwarmed piglets during hypoglycemia.
- Cerebral oxygen consumption (CMRO2) significantly increased in warmed piglets but not in unwarmed piglets.
- Cortical glutamate levels rose during hypoglycemic coma, with a greater increase observed in warmed animals, and normalized rapidly during recovery. EEG recovery was faster in unwarmed animals.
Conclusions:
- Increased CMRO2 and glutamate release during hypoglycemic coma in the immature brain are temperature-dependent.
- Maintaining normothermia during hypoglycemia exacerbates CMRO2 and glutamate release in piglets.
- Therapeutic hypothermia may offer neuroprotection by mitigating excitotoxicity and metabolic distress in immature brains experiencing hypoglycemia.