血栓抑素是一种缓激肽代谢产物，在动脉壁损伤模型中可降低血小板活性。

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

作者信息

Prieto Alejandro R, Ma Hongbao, Huang Ruiping, Khan Gauhar, Schwartz Kenneth A, Hage-Korban Elie E, Schmaier Alvin H, Davis John M, Hasan Ahmed A K, Abela George S

机构信息

Department of Internal Medicine, Division of Cardiology, Michigan State University, East Lansing, MI 48824, USA.

出版信息

Cardiovasc Res. 2002 Mar;53(4):984-92. doi: 10.1016/s0008-6363(01)00514-4.

DOI:10.1016/s0008-6363(01)00514-4

PMID:11922908

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 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.

摘要

目的

凝血酶可激活血小板，并在溶栓治疗或血管成形术后导致动脉阻塞。血栓抑素（RPPGF）是缓激肽的血管紧张素转换酶降解产物，可抑制α-凝血酶诱导的血小板活化。我们推测血栓抑素可预防球囊血管成形术（BA）后血小板的聚集和黏附。

方法

在处死22只比格犬前获取富含血小板的血浆（PRP），并将10%的PRP用111铟标记。然后从每只犬身上取出颈动脉，安装在双灌注室中，通过BA造成内膜损伤。将含或不含血栓抑素或单独使用阿司匹林的111铟-PRP灌注通过动脉60分钟。在灌注过程中，使用库尔特计数器和激光散射技术测量血小板体积。通过放射性计数测量血小板对动脉的黏附。

结果

与未损伤相比，单纯动脉损伤使循环中的血小板体积使用库尔特计数器增加了1.4倍（x）（P<0.05），使用激光散射增加了1.8倍（P<0.05），并使血小板黏附增加了2.3倍（P<0.01）。与单纯BA损伤相比，添加血栓抑素后，使用库尔特计数器测量血小板体积减少了1.8倍（P<0.03），使用激光散射减少了1.9倍（P<0.01），血小板黏附减少了4.2倍（P<0.05）。与单纯BA损伤相比，阿司匹林使血小板体积使用库尔特计数器评估减少了1.2倍（P<0.0１），使用激光散射减少了1.5倍（P<0.03），血小板黏附减少了1.8倍（P<0.02）。