NDLI: Mechanisms of hemorrhagic transformation after tissue plasminogen activator reperfusion therapy for ischemic stroke.

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Mechanisms of hemorrhagic transformation after tissue plasminogen activator reperfusion therapy for ischemic stroke.

Content Provider	Semantic Scholar
Author	Wang, Xiaoying Tsuji, Kiyoshi Lee, Sun-Ryung Ning, Mingming Furie, Karen L. Buchan, Alastair M.
Copyright Year	2004
Abstract	Reperfusion therapy with tissue plasminogen activator (tPA) is a rational therapy for acute ischemic stroke. Properly titrated use of tPA improves clinical outcomes. However, there is also an associated risk of hemorrhagic transformation after tPA therapy. Emerging data now suggest that some of these potentially neurotoxic side effects of tPA may be due to its signaling actions in the neurovascular unit. Besides its intended role in clot lysis, tPA is also an extracellular protease and signaling molecule in brain. tPA mediates matrix remodeling during brain development and plasticity. By interacting with the NMDA-type glutamate receptor, tPA may amplify potentially excitotoxic calcium currents. At selected concentrations, tPA may be vasoactive. Finally, by augmenting matrix metalloproteinase (MMP) dysregulation after stroke, tPA may degrade extracellular matrix integrity and increase risks of neurovascular cell death, blood-brain barrier leakage, edema, and hemorrhage. Understanding these pleiotropic actions of tPA may reveal new therapeutic opportunities for combination stroke therapy.
File Format	PDF HTM / HTML
DOI	10.1161/01.STR.0000143219.16695.af
PubMed reference number	15459442
Journal	Medline
Volume Number	35
Issue Number	11
Alternate Webpage(s)	http://stroke.ahajournals.org/content/strokeaha/35/11_suppl_1/2726.full.pdf?download=true
Alternate Webpage(s)	http://stroke.ahajournals.org/content/strokeaha/35/11_suppl_1/2726.full.pdf
Journal	Stroke
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article

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