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

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Abstract
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 (×) (PPPPPPPPPConclusion: Thrombostatin or aspirin independently decreases evidence of platelet activation in the canine carotid artery model of BA injury.

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