Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/10459
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dc.contributor.authorAbumiya, T.en
dc.contributor.authorFitridge, R.en
dc.contributor.authorMazur, C.en
dc.contributor.authorCopeland, B.en
dc.contributor.authorKoziol, J.en
dc.contributor.authorTschopp, J.en
dc.contributor.authorPierschbacher, M.en
dc.contributor.authordel Zoppo, G.en
dc.date.issued2000en
dc.identifier.citationStroke, 2000; 31(6):1402-1410en
dc.identifier.issn0039-2499en
dc.identifier.issn1524-4628en
dc.identifier.urihttp://hdl.handle.net/2440/10459-
dc.description.abstract<h4>Background and purpose</h4>Platelets become activated and accumulate in brain microvessels of the ischemic microvascular bed after experimental focal cerebral ischemia. The binding of glycoprotein IIb/IIIa (integrin alpha(IIb)beta(3)) on platelets to fibrinogen is the terminal step in platelet adhesion and aggregation. This study tests the hypothesis that inhibition of platelet-fibrin(ogen) interactions may prevent microvascular occlusion after experimental middle cerebral artery occlusion (MCA:O).<h4>Methods</h4>TP9201 is a novel Arg-Gly-Asp (RGD)-containing integrin alpha(IIb)beta(3) inhibitor. Microvascular patency after 3-hour MCA:O and 1-hour reperfusion within the ischemic and nonischemic basal ganglia was compared in adolescent male baboons who received high-dose TP9201 (group A: IC(80) in heparin, n=4), low-dose TP9201 (group B: IC(30) in heparin, n=4), or no treatment (group C: n=4) before MCA:O.<h4>Results</h4>After MCA:O, microvascular patency decreased significantly in group C. However, in the ischemic zones of groups A and B compared with group C, patencies were significantly greater in the 4.0- to 7. 5-microm-diameter (capillary) and 7.5- to 30.0-microm-diameter vessels (2P<0.05). A dose-dependent increase in hemorrhagic transformation was seen in group A (3 of 4 animals) compared with group B (1 of 4 animals), and no hemorrhage was visible in group C (chi(2) analysis for trend, P<0.05).<h4>Conclusions</h4>Platelet activation contributes significantly to ischemic microvascular occlusion. Occlusion formation may be prevented by this RGD-integrin alpha(IIb)beta(3) inhibitor at a dose that does not produce clinically significant parenchymal hemorrhage. The effect of microvascular patency on neuron recovery can now be tested.en
dc.description.statementofresponsibilityTakeo Abumiya, Robert Fitridge, Curt Mazur, Brian R. Copeland, James A. Koziol, Juerg F. Tschopp, Michael D. Pierschbacher, Gregory J. del Zoppo, and Patricia D. Hurnen
dc.language.isoenen
dc.publisherLippincott Williams & Wilkinsen
dc.subjectMicrocirculation; Basal Ganglia; Animals; Papio; Brain Ischemia; Infarction, Middle Cerebral Artery; Cerebral Hemorrhage; Peptides, Cyclic; Oligopeptides; Fibrinogen; Platelet Glycoprotein GPIIb-IIIa Complex; Platelet Aggregation Inhibitors; Reperfusion; Drug Evaluation, Preclinical; Platelet Activation; Vascular Patency; Dose-Response Relationship, Drug; Maleen
dc.titleIntegrin αIIbβ3 inhibitor preserves microvascular patency in experimental acute focal cerebral ischemiaen
dc.title.alternativeIntegrin alphaIIb beta3 inhibitor preserves microvascular patency in experimental acute focal cerebral ischemiaen
dc.typeJournal articleen
dc.identifier.rmid0001001067en
dc.identifier.doi10.1161/01.STR.31.6.1402en
dc.identifier.pubid63410-
pubs.library.collectionSurgery publicationsen
pubs.verification-statusVerifieden
pubs.publication-statusPublisheden
dc.identifier.orcidFitridge, R. [0000-0001-6258-5997]en
Appears in Collections:Surgery publications

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