This Article Full Text Full Text (PDF) All Versions of this Article: 35/9/2220    most recent 01.STR.0000138023.60272.9ev1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Fagan, S. C. Articles by Ergul, A. Search for Related Content PubMed PubMed Citation Articles by Fagan, S. C. Articles by Ergul, A. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Medline Plus Health Information Vasculitis Related Collections Other Stroke Treatment - Medical Endothelium/vascular type/nitric oxide Acute Cerebral Infarction

(Stroke. 2004;35:2220.)
© 2004 American Heart Association, Inc.

Comments, Opinions, and Reviews

Targets for Vascular Protection After Acute Ischemic Stroke

Susan C. Fagan, PharmD; David C. Hess, MD; Elizabeth J. Hohnadel, MS; David M. Pollock, PhD 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, Athens, Ga; the Department of Neurology (S.C.F., D.C.H.) and the Vascular Biology Center (D.M.P., A.E.), Medical College of Georgia, Augusta, Ga; and the Specialty Care Service Line, the Veterans Administration Medical Center (S.C.F., D.C.H.), Augusta, Ga.

Correspondence to Dr Susan C. Fagan, UGA Clinical Pharmacy, CJ-1020 Medical College of Georgia, 1120 15th St, Augusta, GA 30912-2450. 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

This article has been cited by other articles:

				G. Jin, K. Arai, Y. Murata, S. Wang, M. F. Stins, E. H. Lo, and K. van Leyen Protecting Against Cerebrovascular Injury: Contributions of 12/15-Lipoxygenase to Edema Formation After Transient Focal Ischemia Stroke, September 1, 2008; 39(9): 2538 - 2543. [Abstract] [Full Text] [PDF]

				H.-C. Diener, D. Schneider, Y. Lampl, N. M. Bornstein, A. Kozak, G. Rosenberg, and on Behalf of the Study Group DP-b99, a Membrane-Activated Metal Ion Chelator, as Neuroprotective Therapy in Ischemic Stroke Stroke, June 1, 2008; 39(6): 1774 - 1778. [Abstract] [Full Text] [PDF]

				X. Wang, W. H. Baldridge, and B. C. Chauhan Acute Endothelin-1 Application Induces Reversible Fast Axonal Transport Blockade in Adult Rat Optic Nerve Invest. Ophthalmol. Vis. Sci., March 1, 2008; 49(3): 961 - 967. [Abstract] [Full Text] [PDF]

				S. H. Jia, J. Parodo, A. Kapus, O. D. Rotstein, and J. C. Marshall Dynamic Regulation of Neutrophil Survival through Tyrosine Phosphorylation or Dephosphorylation of Caspase-8 J. Biol. Chem., February 29, 2008; 283(9): 5402 - 5413. [Abstract] [Full Text] [PDF]

				T. N. Nagaraja, K. Karki, J. R. Ewing, R. L. Croxen, and R. A. Knight Identification of Variations in Blood-Brain Barrier Opening After Cerebral Ischemia by Dual Contrast-Enhanced Magnetic Resonance Imaging and T1sat Measurements Stroke, February 1, 2008; 39(2): 427 - 432. [Abstract] [Full Text] [PDF]

				H. Taniguchi, I. Mohri, H. Okabe-Arahori, K. Aritake, K. Wada, T. Kanekiyo, S. Narumiya, M. Nakayama, K. Ozono, Y. Urade, et al. Prostaglandin D2 Protects Neonatal Mouse Brain from Hypoxic Ischemic Injury J. Neurosci., April 18, 2007; 27(16): 4303 - 4312. [Abstract] [Full Text] [PDF]

				D. C. Hess NXY-059: A Hopeful Sign in the Treatment of Stroke Stroke, October 1, 2006; 37(10): 2649 - 2650. [Full Text] [PDF]

				N. P.J. Brindle, P. Saharinen, and K. Alitalo Signaling and Functions of Angiopoietin-1 in Vascular Protection Circ. Res., April 28, 2006; 98(8): 1014 - 1023. [Abstract] [Full Text] [PDF]

				M. J. Maneen, R. Hannah, L. Vitullo, N. DeLance, and M. J. Cipolla Peroxynitrite Diminishes Myogenic Activity and Is Associated With Decreased Vascular Smooth Muscle F-Actin in Rat Posterior Cerebral Arteries Stroke, March 1, 2006; 37(3): 894 - 899. [Abstract] [Full Text] [PDF]

				B. Ovbiagele, C. S. Kidwell, S. Starkman, S. L. Selco, V. Rajajee, T. Razinia, and J. L. Saver Angiotensin 2 type 2 receptor activity and ischemic stroke severity Neurology, September 27, 2005; 65(6): 851 - 854. [Abstract] [Full Text] [PDF]

				L. Belayev, I. Saul, R. Busto, K. Danielyan, A. Vigdorchik, L. Khoutorova, and M. D. Ginsberg Albumin Treatment Reduces Neurological Deficit and Protects Blood-Brain Barrier Integrity After Acute Intracortical Hematoma in the Rat Stroke, February 1, 2005; 36(2): 326 - 331. [Abstract] [Full Text] [PDF]