BACKGROUND: Spinal cord injury has been reported after perinatal asphyxia in full-term neonates. OBJECTIVES: To examine the role of excessive nitric oxide production in perinatal spinal cord injury. SUBJECTS AND METHODS: Tissue samples of 18 full-term neonates who died of hypoxic-ischemic encephalopathy were analyzed for the presence of nitrotyrosine (NT). RESULTS: NT was demonstrated in 5 of these 18 neonates. In addition, activated caspase 3, a marker of apoptosis, and CD68, as a marker of inflammation, could be demonstrated in some infants. CONCLUSIONS: excessive nitric oxide production and subsequent NT formation is seen in spinal cord tissue after severe perinatal asphyxia. This finding may be relevant for the development of neuroprotective strategies. Copyright (c) 2007 S. Karger AG, Basel.
BACKGROUND:Spinal cord injury has been reported after perinatal asphyxia in full-term neonates. OBJECTIVES: To examine the role of excessive nitric oxide production in perinatal spinal cord injury. SUBJECTS AND METHODS: Tissue samples of 18 full-term neonates who died of hypoxic-ischemicencephalopathy were analyzed for the presence of nitrotyrosine (NT). RESULTS:NT was demonstrated in 5 of these 18 neonates. In addition, activated caspase 3, a marker of apoptosis, and CD68, as a marker of inflammation, could be demonstrated in some infants. CONCLUSIONS: excessive nitric oxide production and subsequent NT formation is seen in spinal cord tissue after severe perinatal asphyxia. This finding may be relevant for the development of neuroprotective strategies. Copyright (c) 2007 S. Karger AG, Basel.
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