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- eNOS,
- endothelial nitric oxide synthase
- EPO,
- erythropoietin
- H2O2,
- hydrogen peroxide
- HIE,
- hypoxic ischemic encephalopathy
- HI,
- hypoxic-ischemic
- IL,
- interleukin
- NMDA,
- N-methyl-D-aspartate
- nNOS,
- neuron-specific nitric oxide synthase
- NO,
- nitric oxide
- O2−,
- superoxide
- r-EPO,
- recombinant erythropoietin
Abstract
Perinatal hypoxic-ischemic (HI) brain injury is a common problem with potentially devastating impact on neurodevelopmental outcomes. Although therapeutic hypothermia, the first available treatment for this disease, reduces the risk of death or major neurodevelopmental disability, the risk of major neurologic morbidity after HI remains significant. Basic research has identified cellular mechanisms that mediate neuronal death. This article reviews the cellular processes induced that lead to brain injury after HI, and identifies treatments currently under investigation for potential translation to clinical trials.
- Copyright © 2014 by the American Academy of Pediatrics
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