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Cited by 286Nitric Oxide and Endothelin EffectsAcute Ischemic Stroke ManagementNeuroprotection in Cerebral Ischemia

The DOI matches its Crossref record; 34 of the 34 references it cites were found in a registry or an index.

The NOS Inhibitor, 7-Nitroindazole, Decreases Focal Infarct Volume but Not the Response to Topical Acetylcholine in Pial Vessels

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Yoshida, Tazuka, Limmroth, Volker, Irikura, Katsumi, Moskowitz, Michael A.·1994·Journal of Cerebral Blood Flow & Metabolism
DOI 10.1038/jcbfm.1994.123
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Abstract

We examined whether 7-nitroindazole (7-NI), a putative inhibitor of neuronal nitric oxide synthase (nNOS), decreases cerebral infarction 24 h after proximal middle cerebral artery (MCA) occlusion. In preliminary experiments, we determined that 7-NI (25, 50, and 100 mg/kg i.p.) decreased nitric oxide synthase (NOS) activity within cerebral cortex by 40–60% when measured up to 120 min, but not 240 min after administration. At 25 or 50 mg/kg, 7-NI did not alter the systemic arterial blood pressure or the dilation of pial arterioles after topical acetylcholine (10 and 100 μ M). To examine the effect of 7-NI on infarct size, 55 Sprague–Dawley halothaneanesthetized rats were subjected to proximal MCA occlusion (modified Tamura method). Five minutes after occlusion, 7-NI (25 or 50 mg/kg i.p.) or vehicle was injected. Animals treated with 25 or 50 mg/kg showed 25 and 27% reductions in infarct volume, respectively. Coadministration of l-arginine (300 mg/kg i.p.) plus 7-NI (25 mg/kg i.p.) reversed the effect. If, indeed, the effects of 7-NI are mediated by inhibition of nNOS activity, these results suggest that enzymatic products of the neuronal isoform promote ischemic injury and that they do so at least within the first few hours after permanent occlusion. The results also emphasize the importance of developing strategies to selectively inhibit the neuronal isoform inasmuch as we observed previously that administering the less selective NOS inhibitor, N ω -nitro-l-arginine (L-NA), in the same model either caused no change or increased the volume of ischemic injury.

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  1. Morikawa E, 1992, Am J Physiol, 263, H1,632
  2. Moskowitz MA, 1993, Microcirculatory Stasis in the Brain, 287

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Metadata

Authors
Yoshida, T., Limmroth, V., Irikura, K., & Moskowitz, M. A.
Affiliations
Harvard University (US)
ORCID
Venue
Journal of Cerebral Blood Flow & Metabolism
Publisher
SAGE Publications
Published
1994-11
Volume
14
Issue
6
Pages
924-929
ISSN
  • 0271-678X (ISSN-L)
  • 1559-7016
DOI
10.1038/jcbfm.1994.123
OpenAlex
W2047362612
Cited by
286
References
34
Citations by year
2024: 2 · 2022: 2 · 2021: 1 · 2020: 1 · 2019: 1 · 2018: 2 · 2017: 4 · 2016: 1 · 2015: 3 · 2014: 6 · 2013: 3 · 2012: 3
FWCI
16.29
Type
journal article
Language
en
Open access
Licence
journals.sagepub.com/page/policies/text-and-data-mining-license (tdm)
Locations
  • Journal of Cerebral Blood Flow & Metabolism (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r01ns021558-09)
  • National Institute of Neurological Disorders and Stroke (NS-21558, NS 64361)
Topics
  • Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
  • Health Sciences › Medicine › Clinical Neurology › Acute Ischemic Stroke Management
  • Life Sciences › Neuroscience › Neurology › Neuroprotection in Cerebral Ischemia
Keywords
7-nitroindazole, neuronal nitric oxide synthase, nitric oxide, cerebral ischemia, middle cerebral artery occlusion, infarct size, L-arginine, nitric oxide synthase inhibitors, L-NAME, cerebral vasodilation
MeSH terms
Acetylcholine, Administration, Topical, Amino Acid Oxidoreductases, Animals, Brain, Cerebral Infarction, Cerebrovascular Circulation, Indazoles, Male, Pia Mater, Rats, Sprague-Dawley, Nitric Oxide Synthase, Rats

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