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Cited by 131Acute Ischemic Stroke ManagementNeuroprotection in Cerebral IschemiaNeuroinflammation and Neurodegeneration Mechanisms

The DOI matches its Crossref record; 46 of the 46 references it cites were found in a registry or an index.

The Novel β-Blocker, Carvedilol, Provides Neuroprotection in Transient Focal Stroke

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Savitz, Sean I., Erhardt, Joseph A., Anthony, James V., Gupta, Gaurav, Li, Xiang, Barone, Frank C., Rosenbaum, Daniel M.·2000·Journal of Cerebral Blood Flow & Metabolism
DOI 10.1097/00004647-200008000-00005
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Abstract

Increasing evidence supports a role for oxidative stress, proinflammatory cytokines, and apoptosis in the pathophysiology of focal ischemic stroke. Previous studies have found that the multi-action drug, carvedilol, is a mixed adrenergic antagonist, and that it behaves as an antioxidant and inhibits apoptosis. In the current study, the authors investigated whether carvedilol provides protection in focal cerebral ischemia and whether this protection is associated with reduced apoptosis and the downregulation of the inflammatory cytokines, tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). Male Sprague-Dawley rats were subjected to transient middle cerebral artery occlusion (MCAO) by an intraluminal filament technique. Carvedilol (1, 3, and 10 mg/kg) was injected daily subcutaneously 2 or 4 days before the induction of ischemia. Neurologic scores, infarct volumes, TUNEL staining, and mRNA levels of TNF-α and IL-Iβ were assessed at 24 hours reperfusion. The effect of carvedilol on microvascular cortical perfusion was studied with continuous laser—Doppler flowmetry. Twenty-four hours after MCAO, carvedilol at all three doses reduced infarct volumes by at least 40% and reduced neurologic deficits on average by 40% compared with vehicle-treated controls when given 2 or 4 days before the induction of ischemia. This protection was not mediated by changes in temperature or blood flow. Treatment with all three dose regimens resulted in fewer TUNEL positive cells compared with controls. At 24 hours reperfusion, carvedilol decreased TNF-α and IL-1β expression by 40% to 50% in the ipsilateral ischemic cortex compared with the contralateral controls. The results of the current study indicate that carvedilol is neuroprotective in focal cerebral ischemia and may protect the ischemic brain by inhibiting apoptosis and attenuating the expression of TNF-α and IL-1β.

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Research works printed but not linked: 4

  1. Rink A, 1995, Am J Pathol, 147, 1575
  2. Rothwell NJ, 1993, Cerebrovasc Brain Metab Rev, 5, 178
  3. Ruffolo RR, 1998, J Cardiovasc Pharmacol, 32, S22
  4. Yue TL, 1992, J Pharmacol Exp Ther, 263, 92

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Metadata

Authors
Savitz, S. I., Erhardt, J. A., Anthony, J. V., Gupta, G., Li, X., Barone, F. C., & Rosenbaum, D. M.
Affiliations
  • Albert Einstein College of Medicine (US)
  • Department of Cardiovascular Pharmacology, SmithKline Beecham Pharmaceuticals, King of Prussia, Pennsylvania, U.S.A.
  • Yeshiva University (US)
Corresponding author
Rosenbaum, Daniel M.
ORCID
Venue
Journal of Cerebral Blood Flow & Metabolism
Publisher
SAGE Publications
Published
2000-08
Volume
20
Issue
8
Pages
1197-1204
ISSN
  • 0271-678X (ISSN-L)
  • 1559-7016
DOI
10.1097/00004647-200008000-00005
OpenAlex
W2039059620
Cited by
131
References
46
Citations by year
2026: 1 · 2025: 3 · 2024: 5 · 2023: 3 · 2022: 7 · 2021: 7 · 2020: 7 · 2019: 6 · 2018: 8 · 2017: 3 · 2016: 3 · 2015: 6 · 2014: 4 · 2013: 11 · 2012: 6
FWCI
2.15
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
  • National Eye Institute (R01EY011253, EY11253)
  • Division of Materials Research
Topics
  • Health Sciences › Medicine › Clinical Neurology › Acute Ischemic Stroke Management
  • Life Sciences › Neuroscience › Neurology › Neuroprotection in Cerebral Ischemia
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
carvedilol, neuroprotection, focal cerebral ischemia, transient middle cerebral artery occlusion, ischemic stroke, apoptosis, TNF-α, IL-1β, inflammatory cytokines, oxidative stress, infarct size, neurological deficit, microvascular blood flow, TUNEL staining
MeSH terms
Carvedilol, Adrenergic beta-Antagonists, Animals, Brain, Carbazoles, Cerebral Cortex, Cerebral Infarction, Ischemic Attack, Transient, Cerebrovascular Circulation, Interleukin-1, Male, Nervous System, Propanolamines, Tumor Necrosis Factor-alpha, Rats, Sprague-Dawley, Apoptosis, Neuroprotective Agents, Stroke, Rats

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