Beneficial effect of ultra-low-dose aspirin in platelet activity alterations and haemorrhage observed in experimental portal hypertension.

Thrombosis Pub Date : 2012-01-01 Epub Date: 2011-11-14 DOI:10.1155/2012/430460
F X Eizayaga, O Aguejouf, V Desplat, C Doutremepuich
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引用次数: 4

Abstract

Ultra-low-dose aspirin has shown a prothrombotic effect in the laser-induced thrombosis model. Several studies of our laboratory have shown a positive effect in rats with two different experimental models of portal hypertension: portal vein ligation, a model with an almost normal liver, and 30 days of bile duct ligation, a model with cirrhosis and presence of ascitis. In both models of portal hypertensive rats, bleeding time was prolonged and thrombi formation, in a laser-induced model of thrombi production, decreased. The hypotheses of the presented studies were that ultra-low-dose aspirin could decrease the bleeding complications in these models and that the mechanism for these effects could act thorough the COX pathway. In different studies, ultra-low dose of aspirin normalized the induced hemorrhage time, thrombi production, and platelet-endothelial cell interaction. The possible beneficial role of these doses of aspirin and mechanism of COX 2 inhibition are discussed.

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超低剂量阿司匹林对实验性门静脉高压症血小板活性改变和出血的有益作用。
超低剂量阿司匹林在激光致血栓模型中显示出血栓形成前的作用。我们实验室的几项研究表明,在两种不同的门脉高压实验模型的大鼠中,门脉结扎术(肝脏几乎正常的模型)和胆管结扎30天(肝硬化和腹水炎的模型)均有积极作用。在两种门脉高压大鼠模型中,出血时间延长,血栓形成减少,在激光诱导的血栓产生模型中。本研究的假设是,超低剂量阿司匹林可以减少这些模型的出血并发症,其作用机制可能通过COX途径发挥作用。在不同的研究中,超低剂量阿司匹林使诱导出血时间、血栓产生和血小板内皮细胞相互作用正常化。讨论了这些剂量阿司匹林可能的有益作用和抑制COX 2的机制。
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