Herzberg Mark C, Meyer Maurice W
Department of Preventive Sciences, School of Dentistry, University of Minnesota, Minneapolis, MN.
Department of Oral Science.
J Periodontol. 1996 Oct;67 Suppl 10S:1138-1142. doi: 10.1902/jop.1996.67.10s.1138.
During episodes of dental bacteremia, viridans group streptococci encounter platelets. Among these microorganisms, certain induce human and rabbit platelets to aggregate in vitro. In experimental rabbits, circulating streptococci induced platelets to aggregate, triggering the accumulation of platelets and fibrin into the heart valve vegetations of endocarditis. At necropsy, affected rabbit hearts showed ischemie areas. We therefore hypothesized that circulating might cause coronary thrombosis and signs of myocardial infarction (MI). Signs of MI were monitored in rabbits after infusion with platelet-aggregating doses of 4 to 40 × 10 cells of 133-79. Infusion resulted in dose-dependent changes in electrocardiograms, blood pressure, heart rate, and cardiac contractility. These changes were consistent with the occurrence of MI. Platelets isolated from hyperlipidemic rabbits showed an accelerated in vitro aggregation response to strain 133-79. Cultured from immunosuppressed children with septic shock and signs of disseminated intravascular coagulation, more than 60% of isolates of viridans streptococci induced platelet aggregation when tested in vitro. The data are consistent with a thrombogenic role for in human disease, contributing to the development of the vegetative lesion in infective endocarditis and a thrombotic mechanism to explain the additional contributed risk of periodontitis to MI. J Periodontol 1996;67:1138-1142.
在牙源性菌血症发作期间，草绿色链球菌会与血小板相遇。在这些微生物中，某些菌株可在体外诱导人和兔血小板聚集。在实验兔中，循环中的链球菌会诱导血小板聚集，促使血小板和纤维蛋白在感染性心内膜炎的心脏瓣膜赘生物中蓄积。尸检时，受影响的兔心脏出现缺血区域。因此，我们推测循环中的[具体微生物名称未给出]可能会导致冠状动脉血栓形成和心肌梗死（MI）的体征。在用4至40×10个[具体微生物名称未给出] 133 - 79菌株的血小板聚集剂量对兔进行输注后，对MI的体征进行了监测。输注导致心电图、血压、心率和心脏收缩力出现剂量依赖性变化。这些变化与MI的发生一致。从高脂血症兔中分离出的血小板对133 - 79菌株显示出体外聚集反应加速。从患有感染性休克和弥散性血管内凝血体征的免疫抑制儿童中培养出的草绿色链球菌，超过60%的分离株在体外测试时可诱导血小板聚集。这些数据与[具体微生物名称未给出]在人类疾病中的致血栓作用一致，有助于感染性心内膜炎中赘生物病变的发展，以及一种血栓形成机制来解释牙周炎对MI额外增加的风险。《牙周病学杂志》1996年；67:1138 - 1142。
