Endotoxin-Induced Platelet Activation in Human Whole Blood In Vitro

Abstract

SummaryThe effect of purified bacterial endotoxin was studied on human platelets in vitro. In adding up to 1 μg/mL of a highly purified endotoxin, we found neither aggregation nor ATP release in heparinized or citrated human platelet-rich plasma. On the other hand, endotoxin at concentrations as low as a few ng/mL (as may be found in septic patients) caused platelet aggregation in both heparinized and citrated human whole blood, as monitored by change in impedance, free platelet count, and size. Unlike collagen, the platelet aggregation with endotoxin occurred after a long lag phase, developed slowly, and was rarely coupled with measurable release of ATP. The platelet aggregating effect of endotoxin was dose-dependent and modified by exposure of the endotoxin to ionizing radiation. Thus, the activation of human platelets by “solubilized” endotoxin in plasma requires the presence of other blood cells. We propose that the platelet effect is mediated by monocytes and/or neutrophils stimulated by endotoxin.

Comparison of the platelet‐rich plasma and buffy coat protocols for preparation of canine platelet concentrates

“…Also, bacteria can compete with PLT for substrates, including glucose and oxygen. In addition, bacterial endotoxins have been shown to induce PLT aggregation, further reducing contaminated PC quality. This appeared to be the case in one PRP‐PC that had consistent bacterial growth in 3 consecutive samples, either due to contamination during sampling or processing, on days 0 and 1.…”

Glycoprotein IIB/IIIA‐Inhibition and Microcirculatory Alterations During Experimental Endotoxemia—An Intravital Microscopic Study in the Rat

“…The involvement of serotonin and PAF in the development of leukocyte‐independent endothelial damage during endotoxemia focuses the interest to the platelets and a platelet‐endothelial interaction. In early states of sepsis platelets are activated by endotoxin (6) and platelet activating factor (2), and the platelet‐mediated vascular permeability in the rat showed a predominant role for serotonin (10). Platelet activation accompanies the vascular injury seen in septic shock (13,32), and an increase in platelet adhesion to endothelial cells after thrombin treatment or thrombin‐induced platelet activation is well known (20,26).…”

Endotoxin: The uninvited guest

“…Some cells such as leukocytes require minute amounts of LPS to be activated [1] while others such as platelets need a larger concentration [2].…”