CoChat
Sign Up
Cited by 286Nitric Oxide and Endothelin EffectsAcute Ischemic Stroke ManagementNeurological Disorders and Treatments

The NOS inhibitor, 7-nitroindazole, decreases focal infarct volume but not the response to topical acetylcholine in pial vessels

Open access
Yoshida, Tazuka, Limmroth, Volker, Irikura, Katsumi, Moskowitz, Michael A.·1994·Journal of Cerebral Blood Flow & Metabolism
DOI 10.1038/jcbfm.1994.123
Open this paper in CoChat — free accountOpen PDF

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.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1038/jcbfm.1994.123

Cites

34 of 34 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Several studies have linked nitric oxide as a key mediator in numerous neurodegenerative diseases, such as Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis, Huntington's disease and ischemic brain injury.

    “In recent years, several studies have linked nitric oxide as a key mediator in numerous neurodegenerative diseases, such as Parkinson’s disease (PD), Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), Huntington’s disease (HD) and ischemic brain injury (stroke).”

    From The Role of Reactive Species on Innate Immunity (2022) · cites this paper as [145]

  • •NO's dual action makes it a contributing player in pathophysiology and makes development of effective treatments for neurodegenerative diseases particularly difficult.

    “This dual action makes it a contributing player in pathophysiology, but also makes the development of effective treatments for neurodegenerative diseases particularly difficult [141,142,143,144,145].”

    From The Role of Reactive Species on Innate Immunity (2022) · cites this paper as [145]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Research works printed but not linked: 1

  1. Moskowitz MA, Morikawa E, Huang Z, Rosenblatt S, Yoshida T, Irikura K, Dalkara T (1993) L-Arginine infusion promotes nitric oxide-dependent vasodilation in the rat cerebrovascu lature. In: Microcirculatory Stasis in the Brain, New York, Elsevier Science, pp 287-295

Cited by

Sorted by citations

Related

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 › Nitric Oxide and Endothelin Effects
  • Health Sciences › Medicine › Epidemiology › Acute Ischemic Stroke Management
  • Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
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

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review