Abstract
We measured the changes in nitric oxide (NO) metabolites in the brains of neonatal rats with hypoxic-ischemic damage. There were two peaks of NO metabolites in the lesioned side of the cortex without treatment: one during hypoxia and the other during the re-oxygenation period. Prehypoxic treatment with 7-nitroindazole, a selective neuronal NO synthase inhibitor, suppressed both peaks of NO metabolites, whereas prehypoxic treatment with aminoguanidine, a selective inducible NO synthase inhibitor, partially suppressed only the peak in the re-oxygenation period. These data suggest different roles of neuronal and inducible NO synthases in the pathogenesis of hypoxic-ischemic encephalopathy.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
