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on October 6, 2005

Arteriosclerosis, Thrombosis, and Vascular Biology. 2005
Published online before print October 6, 2005, doi: 10.1161/01.ATV.0000189309.05924.88
A more recent version of this article appeared on December 1, 2005
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Submitted on June 16, 2005
Accepted on September 23, 2005

Stimulated Tissue Plasminogen Activator Release as a Marker of Endothelial Function in Humans

James J. Oliver *; David J. Webb ; and David E. Newby

From Centre for Cardiovascular Science (J.J.O., D.J.W., D.E.N.), University of Edinburgh, Edinburgh, UK.

* To whom correspondence should be addressed. E-mail: James.Oliver{at}ed.ac.uk.

Abstract--The initiation, modulation, and resolution of thrombus associated with eroded or unstable coronary plaques are critically dependent on the efficacy of endogenous fibrinolysis. This is dependent on the cellular function of the surrounding endothelium and vascular wall. In particular, the acute release of tissue plasminogen activator from the endothelium makes an important contribution to the defense against intravascular thrombosis. Here, we describe the rationale and methodology for, and clinical relevance of, assessing acute endothelial tissue plasminogen activator release in humans. The investigation of endothelial fibrinolytic function has the potential to provide major new insights into the pathophysiology of cardiovascular disease, and to shape future therapeutic interventions.




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