Levison M E, Carrizosa J, Tanphaichitra D, Schick P K, Rubin W
Blood. 1977 Apr;49(4):645-50.
Because thrombus formation at the site of endothelial injury has been thought to be a critical step in the pathogenesis of bacterial endocarditis, the effect of aspirin on experimental valvular thrombosis and bacterial endocarditis in rabbits was evaluated. Aortic valvular injury and thrombosis were induced in aspirin-treated and control rabbits with intracardiac catheters. A subsequent inoculation of Streptococcus viridans resulted in the development of infective endocarditis. Rabbits were sacrificed as early as 6 hr, and the effectiveness of aspirin was determined by the weight of the sterile vegetations and the quantitation of bacteria in the thrombotic vegetation. Aspirin, in levels in excess of 50 mg/dl did not attenuate the evolution of infective endocarditis, since the formation of sterile thrombotic vegetation and bacterial endocarditis in aspirin-treated rabbits was similar to those in controls.
由于在内皮损伤部位形成血栓被认为是细菌性心内膜炎发病机制中的关键步骤，因此评估了阿司匹林对兔实验性瓣膜血栓形成和细菌性心内膜炎的影响。通过心内导管在服用阿司匹林的兔和对照兔中诱导主动脉瓣膜损伤和血栓形成。随后接种草绿色链球菌导致感染性心内膜炎的发生。最早在6小时处死兔子，并通过无菌赘生物的重量和血栓性赘生物中的细菌定量来确定阿司匹林的有效性。超过50mg/dl水平的阿司匹林并未减弱感染性心内膜炎的发展，因为服用阿司匹林的兔中无菌血栓性赘生物和细菌性心内膜炎的形成与对照组相似。
