Eizayaga F X, Aguejouf O, Desplat V, Doutremepuich C
Laboratoire d'Hématologie, UFR des Sciences Pharmaceutiques, Université de Bordeaux 2, Victor Segalen, 33076 Bordeaux Cedex, France.
Thrombosis. 2012;2012:430460. doi: 10.1155/2012/430460. Epub 2011 Nov 14.
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.
超低剂量阿司匹林在激光诱导血栓形成模型中显示出促血栓形成作用。我们实验室的多项研究表明,在两种不同的门静脉高压实验模型大鼠中,超低剂量阿司匹林具有积极作用:门静脉结扎模型(肝脏几乎正常)和胆管结扎30天模型(肝硬化且有腹水)。在这两种门静脉高压大鼠模型中,出血时间延长,而在激光诱导血栓形成模型中,血栓形成减少。上述研究的假设是,超低剂量阿司匹林可减少这些模型中的出血并发症,且这些作用的机制可能通过COX途径发挥作用。在不同研究中,超低剂量阿司匹林使诱导的出血时间、血栓形成及血小板-内皮细胞相互作用恢复正常。文中讨论了这些剂量阿司匹林可能的有益作用及COX 2抑制机制。