Skip Navigation

Cardiovascular Research 2002 53(4):984-992; doi:10.1016/S0008-6363(01)00514-4
© 2002 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Prieto, A. R
Right arrow Articles by Abela, G. S
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Prieto, A. R
Right arrow Articles by Abela, G. S
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2002, European Society of Cardiology

Thrombostatin, a bradykinin metabolite, reduces platelet activation in a model of arterial wall injury

Alejandro R Prietoa, Hongbao Maa, Ruiping Huanga, Gauhar Khana, Kenneth A Schwartza, Elie E Hage-Korbana, Alvin H Schmaierb,c, John M Davisa, Ahmed A.K Hasanb,c and George S Abelaa,*

aDepartment of Internal Medicine, Divisions of Cardiology and Hematology and Oncology, Michigan State University, East Lansing, MI, USA
bDepartment of Internal Medicine, University of Michigan, Ann Arbor, MI, USA
cThromgen, Inc., Ann Arbor, MI, USA

* Corresponding author. Present address: Department of Medicine/Cardiology, Michigan State University, B-208 Clinical Center, East Lansing, MI 48824, USA. Tel.: +1-517-353-4832; fax: +1-517-432-4039 abela{at}pilot.msu.edu

Objective: Thrombin activates platelets and contributes to the occlusion of arteries following thrombolytic therapy or angioplasty. Thrombostatin (RPPGF), the angiotensin converting enzyme degradation product of bradykinin, inhibits {alpha}-thrombin induced platelet activation. We hypothesized that thrombostatin prevents platelet aggregation and adhesion after balloon angioplasty (BA). Methods: Platelet-rich plasma (PRP) was obtained from 22 Beagle dogs before sacrifice and 10% of the PRP was labeled with 111In. Carotid arteries were then removed from each dog and mounted in a dual perfusion chamber and intimal injury was performed with BA. 111In-PRP with or without thrombostatin or aspirin alone was perfused through the arteries for 60 min. During perfusion, platelet volume was measured using a Coulter counter and a laser-light scattering technique. Platelet adhesion to arteries was measured by radioactivity count. Results: Arterial injury alone compared to non-injury increased platelet volume in the circuit by 1.4 times (x) (P<0.05) using a Coulter counter or 1.8x (P<0.05) using laser-light scattering and increased platelet adhesion by 2.3x (P<0.01). When compared to BA injury alone, the addition of thrombostatin reduced platelet volume by 1.8x (P<0.03) as measured by Coulter counter or 1.9x (P<0.01) by laser-light scattering and platelet adhesion by 4.2x (P<0.05). Compared to BA injury alone, aspirin reduced platelet volume by 1.2x (P<0.01) as assessed by Coulter counter or 1.5x (P<0.03) using laser-light scattering and platelet adhesion by 1.8x (P<0.02). Conclusion: Thrombostatin or aspirin independently decreases evidence of platelet activation in the canine carotid artery model of BA injury.

KEYWORDS Angioplasty; Anticoagulants; Arteries; Platelets; Thrombosis/embolism


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.