Nitric oxide in early brain injury after subarachnoid hemorrhage

Fatima A. Sehba, Joshua B. Bederson

Research output: Chapter in Book/Report/Conference proceedingConference contributionpeer-review

34 Scopus citations


Nitric Oxide (NO) is the major regulator of cerebral blood flow. In addition, it inhibits platelet adherence and aggregation, reduces adherence of leukocytes to the endothelium, and suppresses vessel injury. NO is produced on demand by nitric oxide synthase and has a very short half life. Hence maintenance of its cerebral level is crucial for normal vascular physiology. Time dependent alterations in cerebral NO level and the enzymes responsible for its synthesis are found after subarachnoid hemorrhage (SAH). Cerebral NO level decreases, recovers and increases within the first 24h after SAH. Each change in cerebral NO level elicits a different pathological response form already compromised brain. These response range from constriction, platelet aggregation and vascular injury that occurs during the early hours and delayed occurring vasospasm, neuronal and axonal damage. This review summarizes the underlying mechanism and the consequence of alteration in cerebral NO level on brain during the first 72h after SAH.

Original languageEnglish
Title of host publicationEarly Brain Injury or Cerebral Vasospasm
Subtitle of host publicationVolume 1: Pathophysiology
PublisherSpringer-Verlag Wien
Number of pages5
ISBN (Print)9783709103524
StatePublished - 2011

Publication series

NameActa Neurochirurgica, Supplementum
ISSN (Print)0065-1419
ISSN (Electronic)0001-6268


  • Early brain injury
  • Nitric oxide
  • Vasospasm


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