Semeraro N, Fumarola D, Telesforo P, Vermylen J
Boll Ist Sieroter Milan. 1976;55(6):577-86.
The studies reviewed in the present manuscript outline the effects of bacterial endotoxins on human and animal platelets. In animals the endotoxin administration is followed by thrombocytopenia, presence of platelet aggregates in the blood vessels of several organs, appearance of appreciable quantities of serotonin in plasma and increased platelet factor 3 availability. These in vivo effects can readily be explained by the in vitro demonstration that endotoxin aggregates platelets, induces release of vasoactive amines and adenine nucleotides and activates platelet factor 3. There is substantial evidence suggesting that the mechanism of this animal platelet-endotoxin interaction is immunological and complement dependent. In humans thrombocytopenia is frequently observed in endotoxemia as encountered during Gram-negative sepsis indicating that platelets are involved in some of the biological effects endotoxin. In vitro experiments demonstrate that several endotoxin preparations significantly enhance a weak procoagulant activity of human platelets different from platelet factor 3.
本手稿中综述的研究概述了细菌内毒素对人和动物血小板的影响。在动物中，给予内毒素后会出现血小板减少、多个器官血管中存在血小板聚集体、血浆中出现大量血清素以及血小板因子3可用性增加。这些体内效应很容易通过体外实验得到解释，即内毒素可使血小板聚集、诱导血管活性胺和腺嘌呤核苷酸释放并激活血小板因子3。有大量证据表明，这种动物血小板与内毒素相互作用的机制是免疫性的且依赖补体。在人类中，革兰氏阴性菌败血症期间出现的内毒素血症常伴有血小板减少，这表明血小板参与了内毒素的某些生物学效应。体外实验表明，几种内毒素制剂可显著增强人血小板不同于血小板因子3的微弱促凝活性。
