The Double Role of Nitric Oxide Synthase in Reperfusion Following Focal Cerebral Ischemia

Objective To study the expression of three isoforms of nitric oxide synthase (NOS) after transient cerebral ischemia-reperfusion in rat, and provide theoreticalbasisfortherapy.Methods In a model of reversible middle cerebral artery occlusion through monofilament nylon suture, by three isoforms of NOS polyclone antibody-SP immunochemisty technique, the expression of neuronal NOS (nNOS), inducible NOS (iNOS) and endothelial NOS (eNOS) after ischemia 2 h plus reperfusion 15 min and ischemia 2 h plus reperfusion for 22 h were detected. Results (1) 15 min reperfusion following 2 h ischemia, eNOS immunoreactivity in blood vesselsandneuronsattheborder of ischemic territory was upregulated. (2) 22 h reperfusion following 2 h ischemia, theexpressionofnNOSwasdownregulated within the infracted region and iNOS immunoreactivity were observed in glial cells infiltrating the infracted region.eNOSand iNOS immunoreactivitywereupregu- lated in blood vessels and neurons at the border of infarcted region. Conclusions The upregulated expression of eNOS in the early phase of reperfusion following transient ischemia may play a protective role at the border of ischemic territory;In the later phase of reperfusion the neuroprotective role of eNOS and the neurodegenetive role of iNOS are coexisting. So itsupportthehypothesisthattheselectiveiNOSinhibitors and/or eNOS enhancer may be useful to reduce the delayed cerebral ischemic injury.