Nystrom M L, Barradas M A, Jeremy J Y, Mikhailidis D P
Department of Chemical Pathology and Human Metabolism, Royal Free Hospital, School of Medicine, University of London, UK.
Thromb Haemost. 1994 May;71(5):646-50.
The effect of endotoxic lipopolysaccharide (LPS) on platelet shape change (PSC; a preaggregation event) was investigated. PSC is accompanied by an increase in median platelet volume (MPV), which was measured using a channelyzer. In whole blood, but not in platelet rich plasma (PRP), LPS (final concentration 80 mg/l) caused an increase in MPV that could be detected for 2 h. When PRP (prepared from LPS- and saline-pretreated whole blood) was incubated for 40 min, the LPS-mediated increase in MPV could no longer be detected. Taken together, these data imply that PSC is both initiated and maintained by a labile factor(s) present in whole blood, but not in PRP. PRP was prepared from LPS-pretreated whole blood and incubated for 40 min to allow reversal of the LPS-induced PSC; further stimulation with LPS caused PSC. Platelets from LPS-pretreated whole blood also showed enhanced PSC with serotonin (5-HT), diminished PSC with platelet activating factor (PAF), and no change of response to ADP and collagen. Hence, LPS pretreatment of whole blood differentially alters responses of platelets to further stimulation with LPS and other agonists. A specific PAF antagonist completely abolished the effect of LPS on MPV. These data may contribute to an understanding of the cascading thrombotic events and thrombocytopenia associated with septicaemia.
研究了内毒素脂多糖（LPS）对血小板形状变化（PSC；一种预聚集事件）的影响。PSC伴随着血小板平均体积（MPV）的增加，MPV使用通道分析仪进行测量。在全血中，但不在富血小板血浆（PRP）中，LPS（终浓度80mg/l）导致MPV增加，这种增加可持续2小时。当将PRP（由LPS和生理盐水预处理的全血制备）孵育40分钟时，不再能检测到LPS介导的MPV增加。综上所述，这些数据表明PSC由全血中存在但PRP中不存在的不稳定因子启动并维持。PRP由LPS预处理的全血制备，并孵育40分钟以使LPS诱导的PSC逆转；用LPS进一步刺激导致PSC。来自LPS预处理全血的血小板对5-羟色胺（5-HT）也表现出增强的PSC，对血小板活化因子（PAF）表现出减弱的PSC，对ADP和胶原的反应无变化。因此，全血的LPS预处理差异性地改变血小板对LPS和其他激动剂进一步刺激的反应。一种特异性PAF拮抗剂完全消除了LPS对MPV的作用。这些数据可能有助于理解与败血症相关的级联血栓形成事件和血小板减少症。
