ArticleExperimental neurology2014
Transient ischemia elicits a sustained enhancement of thrombus development in the cerebral microvasculature: effects of anti-thrombotic therapy.
Article in Experimental neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Delayed plasma kallikrein inhibition fosters post-stroke recovery by reducing thrombo-inflammation.Journal of neuroinflammation · 2024Article
- Thromboinflammatory challenges in stroke pathophysiology.Seminars in immunopathology · 2023Review
- Platelet depletion does not alter long-term functional outcome after cerebral ischaemia in mice.Brain, behavior, & immunity - health · 2022Article
- Dl-3-N-Butylphthalide Promotes Angiogenesis in an Optimized Model of Transient Ischemic Attack in C57BL/6 Mice.Frontiers in pharmacology · 2021Article
- Animal models of transient ischemic attack: a review.Acta neurologica Belgica · 2020Review
- The isothiocyanate sulforaphane modulates platelet function and protects against cerebral thrombotic dysfunction.British journal of pharmacology · 2018Article
- Interleukin-6 mediates enhanced thrombus development in cerebral arterioles following a brief period of focal brain ischemia.Experimental neurology · 2015Article
- Article
- A possible new focus for stroke treatment - migrating stem cells.Expert opinion on biological therapy · 2015Review
- Angioplasty and stenting for severe vertebral artery orifice stenosis: effects on cerebellar function remodeling verified by blood oxygen level-dependent functional magnetic resonance imaging.Neural regeneration research · 2014Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
objectiveWhile transient ischemic attack (TIA) is a well-known harbinger of ischemic stroke, the mechanisms that link TIA to subsequent strokes remain poorly understood. The overall aim of this study was to determine whether: 1) brief periods of transient cerebral ischemia render this tissue more vulnerable to thrombus development and 2) antiplatelet agents used in TIA patients alter ischemia-induced thrombogenesis. APPROACH &
resultsThe middle cerebral artery of C57BL/6 mice was occluded for 2.5-10min, followed by reperfusion periods of 1-28days. Intravital microscopy was used to monitor thrombus development in cerebral microvessels induced by light/dye photoactivation. Thrombosis was quantified as the time to platelet aggregation on the vessel wall and the time for complete blood flow cessation. While brief periods of cerebral ischemia were not associated with neurological deficits or brain infarction (evaluated after 1day), it yielded a pronounced and prolonged (up to 28days) acceleration of thrombus formation, compared to control (sham) mice. This prothrombotic phenotype was not altered by pre- and/or post-treatment of mice with either aspirin (A), clopidogrel (C), dipyridamole (D), or atorvastatin (S), or with A+D+S.
conclusionsThe increased vulnerability of the cerebral vasculature to thrombus development after a brief period of transient ischemia can be recapitulated in a murine model. Antiplatelet or antithrombotic agents used in patients with TIA show no benefit in this mouse model of brief transient ischemia.
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