Glucose, lactic acid, and perinatal hypoxic-ischemic brain damage.
Investigations suggest that hyperglycemia, superimposed on hypoxia-ischemia or cerebral ischemia, accentuates brain damage in adult experimental animals and humans, but not in immature animals. Fundamental differences in the immature and adult brain, which account for the age-specific paradox, are discussed. Based on currently available data, we recommend that glucose supplementation not be curtailed during labor and delivery of asphyxiated human infants; on the contrary, glucose therapy may substantially reduce hypoxic-ischemic brain damage.
Vannucci
R C
RC
Division of Pediatric Neurology, Milton S. Hershey Medical Center, Hershey, PA 17033.
Yager
J Y
JY
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D001921:Brain / Q000503:physiopathology; D001925:Brain Damage, Chronic / Q000503:physiopathology* / Q000628:therapy; D004734:Energy Metabolism / Q000502:physiology; D005311:Fetal Hypoxia / Q000503:physiopathology* / Q000628:therapy; D005950:Glucose Solution, Hypertonic / Q000008:administration & dosage; D006801:Humans; D007231:Infant, Newborn; D007773:Lactates / Q000097:blood*; D019344:Lactic Acid
D001786:Blood Glucose; D005950:Glucose Solution, Hypertonic; D007773:Lactates; D019344:Lactic Acid