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

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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 α-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 (×) (P<0.05) using a Coulter counter or 1.8× (P<0.05) using laser-light scattering and increased platelet adhesion by 2.3× (P<0.01). When compared to BA injury alone, the addition of thrombostatin reduced platelet volume by 1.8× (P<0.03) as measured by Coulter counter or 1.9× (P<0.01) by laser-light scattering and platelet adhesion by 4.2× (P<0.05). Compared to BA injury alone, aspirin reduced platelet volume by 1.2× (P<0.01) as assessed by Coulter counter or 1.5× (P<0.03) using laser-light scattering and platelet adhesion by 1.8× (P<0.02). Conclusion: Thrombostatin or aspirin independently decreases evidence of platelet activation in the canine carotid artery model of BA injury. © 2002 Elsevier Science B.V. All rights reserved.




Prieto, A. R., Ma, H., Huang, R., Khan, G., Schwartz, K. A., Hage-Korban, E. E., … Abela, G. S. (2002). Thrombostatin, a bradykinin metabolite, reduces platelet activation in a model of arterial wall injury. Cardiovascular Research, 53(4), 984–992.

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