Key result
Addition of bacterial lipopolysaccharide to whole blood consistently enhanced platelet aggregation and increased median platelet volume, an effect inhibited by the calcium channel blocker verapamil.
Why the study?
Does bacterial lipopolysaccharide activate human platelets in whole blood?
Does bacterial lipopolysaccharide activate human platelets in whole blood?
LPS activates platelets in whole blood but not in platelet-rich plasma, likely mediated by other blood cells and dependent on calcium influx.
Answers are grounded in this paper and cite their sources.
LPS effects on platelets in whole blood may warrant further study; leaves open any role in human sepsis or verapamil use.
The addition of lipopolysaccharide (LPS) from Gram-negative bacteria to whole blood induced a consistent enhancement of platelet impedance aggregation (WB-PIA) and an increase in median platelet volume (MPV). In contrast, the addition of LPS to platelet rich plasma (PRP) resulted in inconsistent changes in turbidometric platelet aggregation (TPA) and no significant change in MPV. The LPS-induced increase of MPV in whole blood was inhibited by verapamil, a calcium channel blocker. We conclude that: (a) LPS consistently activates platelets in whole blood but not in PRP; (b) LPS-induced activation of platelets is probably mediated by products released by leucocytes and/or erythrocytes; (c) the increase in MPV induced by LPS is probably dependent upon calcium influx; and (4) an increase in MPV may be a useful and sensitive model for the study of platelet activation by LPS, in vitro and in vivo.
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Whitworth et al. (1989) studied this question. Lipopolysaccharide (LPS) was evaluated on Platelet impedance aggregation (WB-PIA) and median platelet volume (MPV). Addition of bacterial lipopolysaccharide to whole blood consistently enhanced platelet aggregation and increased median platelet volume, an effect inhibited by the calcium channel blocker verapamil.
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