[The role of nitric oxide in hypoxic-ischemic injury]

It has been shown that nitric oxide (NO) generating cells are distributed widely in the brain and NO may act both as a neurodestructive and a neuroprotective agent in the pathogenesis of hypoxic-ischemic and reoxygenation injuries. Induction of hypoxia-ischemia dramatically increases NO production in brain. It is supposed that neuronally derived NO mediates glutamate neurotoxicity. The reaction of NO with superoxide can lead to neurotoxicity through formation of peroxynitrite which decomposes to form the cytotoxic oxygen free radical. On the other hand, NO mediates vasorelaxation and anti-thrombopoietic property and may protect against ischemic injury in this aspect. Some NO donors may also act as a protective agent through downregulation of NMDA receptor activity. These current studies suggest that some selective NO synthesis inhibitors or NO donors could be used in the novel treatment of hypoxic-ischemic brain injury.