Published Online
on July 29, 2004

A more recent version of this article appeared on September 1, 2004

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Submitted on March 29, 2004
Revised on June 10, 2004
Accepted on June 15, 2004

Targets for Vascular Protection After Acute Ischemic Stroke

Susan C. Fagan PharmD^*; David C. Hess MD; Elizabeth J. Hohnadel MS; David M. Pollock PhD; and Adviye Ergul MD, PhD

From the Program in Clinical and Experimental Therapeutics (S.C.F., E.J.H., A.E.), College of Pharmacy, University of Georgia; the Department of Neurology (S.C.F., D.C.H.) and the Vascular Biology Center (D.M.P., A.E.), Medical College of Georgia; and the Specialty Care Service Line, the Veterans Administration Medical Center (S.C.F., D.C.H.), Augusta, Ga.

^* To whom correspondence should be addressed. E-mail: sfagan{at}mail.mcg.edu.

Background--Vascular damage caused by cerebral ischemia leads to edema, hemorrhage formation, and worsened outcomes in ischemic stroke patients. Therapeutic interventions need to be developed to provide vascular protection. The purpose of this review is to identify the pathophysiologic processes involved in vascular damage after ischemia, which may lead to strategies to provide vascular protection in ischemic stroke patients.

Summary of Comment--The pathologic processes caused by vascular injury after an occlusion of a cerebral artery can be separated into acute (hours), subacute (hours to days), and chronic (days to months). Targets for intervention can be identified for all 3 stages. Acutely, superoxide is the predominant mediator, followed by inflammatory mediators and proteases subacutely. In the chronic phase, proapoptotic gene products have been implicated.

Conclusions--Pharmacological agents designed to target specific pathologic and protective processes affecting the vasculature should be used in clinical trials of vascular protection after acute ischemic stroke.

Key words: cerebral ischemia, focal • clinical trials • free radicals • ischemia • pharmacology

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