Article detail · 1994
Effects of cerebral ischemia in mice deficient in neuronal nitric oxide synthase
- Year
- 1994
- Type
- article
Data source split
- YÖKSİS YÖKSİS article record
- YÖKSİS venue Science
- Catalog match (ISSN) Science
- OpenAlex OpenAlex enrichment (abstract, citations, topics)
Abstract
OpenAlex · English
The proposal that nitric oxide (NO) or its reactant products mediate toxicity in brain remains controversial in part because of the use of nonselective agents that block NO formation in neuronal, glial, and vascular compartments. In mutant mice deficient in neuronal NO synthase (NOS) activity, infarct volumes decreased significantly 24 and 72 hours after middle cerebral artery occlusion, and the neurological deficits were less than those in normal mice. This result could not be accounted for by differences in blood flow or vascular anatomy. However, infarct size in the mutant became larger after endothelial NOS inhibition by nitro-L-arginine administration. Hence, neuronal NO production appears to exacerbate acute ischemic injury, whereas vascular NO protects after middle cerebral artery occlusion. The data emphasize the importance of developing selective inhibitors of the neuronal isoform.
Topics
Citations
OpenAlex cited_by_count. Not a WoS or Scopus citation count; those sources have no separate column here.
1,581 citations
OpenAlex cited_by_count (cache / database)
49 publications in the local catalog that cite this work (OpenAlex reference match; not the full global list).
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