An investigation into the effects of bacterial lipopolysaccharide on human platelets.
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.
Whitworth
N H
NH
Department of Chemical Pathology and Human Metabolism, Royal Free Hospital, London, UK.
Barradas
M A
MA
Mikhailidis
D P
DP
Dandona
P
P
D001772:Blood Cell Count; D001792:Blood Platelets / Q000187:drug effects*; D005340:Fibrinogen / Q000032:analysis; D006801:Humans; D066298:In Vitro Techniques; D008070:Lipopolysaccharides / Q000494:pharmacology*; D010314:Partial Thromboplastin Time; D015539:Platelet Activation / Q000187:drug effects; D010974:Platelet Aggregation / Q000187:drug effects; D011517:Prothrombin Time
D008070:Lipopolysaccharides; D005340:Fibrinogen