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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.

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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:

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  • 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.