Whole blood impedance aggregometry findings in experimental endotoxinemia
© BioMed Central Ltd 2013
Published: 17 April 2013
In an observational study in a recent issue of Critical Care, we demonstrated that platelet function, as assessed by impedance aggregometry, is reduced in patients with severe sepsis and poor prognosis . In the present study, we investigated whether the prototypic endotoxin lipopolysaccharide (LPS) (Escherichia coli; serotype 0.111:B4; Sigma-Aldrich, Munich, Germany) exerts comparable effects in an in vitro model. Therefore, heparinized blood samples were drawn from the antecubital vein of healthy probands. After incubation of samples with LPSs (100 μg/mL) or vehicle for 240 minutes at 37°C, samples were subjected to impedance aggregometry (Roche Diagnostics Deutschland GmbH, Mannheim, Germany), and aggregation was induced by adenosine diphosphate (ADP), collagen, thrombin receptor-activating peptide (TRAP), or arachidonic acid.
Our in vitro findings on LPS-induced inhibition of platelet aggregation closely agree with our recent observational study in patients with severe sepsis. In both studies, the decrease in platelet function was dependent on the activator used and the ranking of activators was identical (collagen > TRAP > ADP). Moreover, our finding that LPS did not reduce arachidonic acid-induced platelet aggregation is in agreement with our previous observational study. In contrast to the other activators, arachidonic acid was neither an independent predictor of the diagnosis of severe sepsis nor an independent predictor of the outcome in severe sepsis.
Thus, the present study demonstrates that the decrease in platelet aggregation seen in patients with severe sepsis can be mimicked in the in vitro setting, suggesting comparable pathophysiological mechanisms.
thrombin receptor-activating peptide.
Approval of the ethics committee (University Hospital Essen) and consent of the healthy probands were obtained. The authors declare that funding for this report was solely departmental.