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Binding of hydroxyethyl starch molecules to the platelet surface
Engelbert Deusch1, Thomas Gamsjäger, Hans-Georg Kress
1Department of Anesthesiology and Intensive Care (B), University of Vienna, School of Medicine, Vienna, Austria.
Anesthesia and Analgesia
|August 23, 2003
Summary
Hydroxyethyl starch (HES) solutions reduce platelet function by coating platelets, not through intracellular pathways. This surface binding blocks the fibrinogen receptor, explaining HES
Area of Science:
- Biochemistry
- Hematology
- Pharmacology
Background:
- Hydroxyethyl starch (HES) solutions are known to impair platelet function.
- Previous research suggested HES effects are not mediated by intracellular signaling.
- A hypothesis proposed unspecific HES macromolecule coating of platelets causes antiplatelet effects.
Purpose of the Study:
- To investigate the binding of fluorochrome-coupled HES to human platelet surfaces.
- To determine if extracellular HES binding is responsible for its antiplatelet effects.
Main Methods:
- Whole blood flow cytometry was used to analyze HES binding to platelets.
- Citrated whole blood from volunteers was incubated with fluorescein isothiocyanate (FITC)-coupled HES.
- FITC-positive platelets were quantified using flow cytometry at varying hemodilution levels.
Main Results:
- FITC-HES binding to platelets increased in a concentration-dependent manner.
- Significant binding was observed at 10% hemodilution.
- HES binding was independent of fibrinogen receptor blockade.
Conclusions:
- Extracellular binding of HES to the platelet surface is demonstrated.
- This binding partially explains the antiplatelet effects of HES.
- HES binding blocks ligand access to the platelet fibrinogen receptor.