Experimental biology of cerebral hypoxia-ischemia: relation to perinatal brain damage.
Cerebral hypoxia-ischemia remains a major cause of acute perinatal brain injury, leading ultimately to neurologic dysfunction manifest as cerebral palsy, mental retardation, and epilepsy. Research in experimental animals over the past 10 or more years has expanded greatly our understanding of the cellular and molecular events that occur during a hypoxic-ischemic insult to brain, and recent discoveries have suggested that metabolic perturbations arising in the recovery period after resuscitation contribute substantially to the nature and extent of neuronal destruction. The review focuses on those neurochemical processes responsible for the maintenance of cellular homeostasis and how these mechanisms fail in hypoxia-ischemia to culminate in brain damage. Knowledge of these critical events has opened new avenues of potential therapy for the fetus and newborn infant subjected to cerebral hypoxia-ischemia to prevent the serious delayed effects of perinatal brain injury.
Vannucci
R C
RC
Division of Pediatric Neurology, Milton S. Hershey Medical Center, Pennsylvania State University, Hershey 17033.
D000818:Animals; D000831:Animals, Newborn; D001930:Brain Injuries / Q000209:etiology* / Q000378:metabolism; D002545:Brain Ischemia / Q000209:etiology* / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D004734:Energy Metabolism; D005609:Free Radicals; D006706:Homeostasis; D006801:Humans; D002534:Hypoxia, Brain / Q000209:etiology* / Q000378:metabolism; D007231:Infant, Newborn; D018377:Neurotransmitter Agents / Q000378:metabolism; D015290:Second Messenger Systems / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology
D005609:Free Radicals; D018377:Neurotransmitter Agents; D002118:Calcium