Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Acute decrease in cerebral nitric oxide levels after subarachnoid hemorrhage.

F A Sehba1, A Y Schwartz, I Chereshnev

  • 1Department of Neurosurgery, Mount Sinai School of Medicine, New York, New York 10029-6574, USA.

Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism
|March 21, 2000
PubMed
Summary

Subarachnoid hemorrhage (SAH) acutely reduces nitric oxide (NO) availability in the brain, contributing to vasoconstriction and ischemia. This study shows SAH directly depletes NO metabolites, independent of nitric oxide synthase inhibition.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Early platelet activation, inflammation and acute brain injury after a subarachnoid hemorrhage: a pilot study.

Journal of thrombosis and haemostasis : JTH·2012
Same author

Seizures after Onyx embolization for the treatment of cerebral arteriovenous malformation.

Interventional neuroradiology : journal of peritherapeutic neuroradiology, surgical procedures and related neurosciences·2011
Same author

Reporting standards for endovascular repair of saccular intracranial cerebral aneurysms.

AJNR. American journal of neuroradiology·2010
Same author

Escape of intraluminal platelets into brain parenchyma after subarachnoid hemorrhage.

Neuroscience·2009
Same author

A rare spontaneous osteosarcoma of the calvarium in a patient with long-standing fibrous dysplasia: CT and MR findings.

The British journal of radiology·2008
Same author

Clinical improvement related to thrombolysis of third ventricular blood clot in a patient with thalamic hemorrhage.

Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association·2007

Area of Science:

  • Neuroscience
  • Vascular Biology
  • Biochemistry

Background:

  • Disturbances in the nitric oxide (NO) pathway are linked to vasoconstriction and ischemia post-subarachnoid hemorrhage (SAH).
  • The hypothesis is that blood from SAH scavenges NO, reducing its availability and causing vasoconstriction.

Purpose of the Study:

  • To investigate the impact of SAH on NO metabolite levels in different brain regions.
  • To determine if SAH-induced vasoconstriction is mediated by NO scavenging.

Main Methods:

  • Measurement of nitrite and nitrate (NO metabolites) in five brain regions before and after experimental SAH.
  • Administration of a nitric oxide synthase (NOS) inhibitor in sham-operated animals to assess its effect on NO metabolites.

Main Results:

Related Experiment Videos

  • SAH significantly decreased NO metabolites in most brain regions within 10 minutes, except the hippocampus.
  • Nitrite levels recovered, but nitrate remained decreased in specific brain regions (brain stem, ventral cortex) post-SAH.
  • NOS inhibition showed a delayed decrease in NO metabolites, distinct from the acute SAH effect.

Conclusions:

  • SAH causes acute reductions in cerebral NO levels through a mechanism independent of NOS inhibition.
  • These findings support the hypothesis that altered NO availability contributes directly to ischemic injury following SAH.