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HES 130/0.4 impairs haemostasis and stimulates pro-inflammatory blood platelet function

INTRODUCTION: Hydroxyethyl starch (HES) solutions are widely used for volume replacement therapy but are also known to compromise coagulation, impair renal function and increase long-term mortality. To test the hypotheses that HES 130/0.4 has fewer adverse effects than HES 200/0.5 and exerts anti-in...

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Autores principales: Sossdorf, Maik, Marx, Sascha, Schaarschmidt, Barbara, Otto, Gordon P, Claus, Ralf A, Reinhart, Konrad, Hartog, Christiane S, Lösche, Wolfgang
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2811952/
https://www.ncbi.nlm.nih.gov/pubmed/20028511
http://dx.doi.org/10.1186/cc8223
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author Sossdorf, Maik
Marx, Sascha
Schaarschmidt, Barbara
Otto, Gordon P
Claus, Ralf A
Reinhart, Konrad
Hartog, Christiane S
Lösche, Wolfgang
author_facet Sossdorf, Maik
Marx, Sascha
Schaarschmidt, Barbara
Otto, Gordon P
Claus, Ralf A
Reinhart, Konrad
Hartog, Christiane S
Lösche, Wolfgang
author_sort Sossdorf, Maik
collection PubMed
description INTRODUCTION: Hydroxyethyl starch (HES) solutions are widely used for volume replacement therapy but are also known to compromise coagulation, impair renal function and increase long-term mortality. To test the hypotheses that HES 130/0.4 has fewer adverse effects than HES 200/0.5 and exerts anti-inflammatory properties, we compared the effects of HES 130/0.4, HES 200/0.5 and saline on in vitro haemostasis and pro-inflammatory platelet function. METHODS: Whole blood samples from healthy volunteers were mixed with 6% HES 130/0.4, 10% HES 200/0.5, or normal saline to achieve a final haemodilution rate of 10% or 40%. Haemostatic capacity was characterised by thromboelastography (ROTEM) and measurement for FXIIIa activity. Platelet activation and pro-inflammatory platelet functions were characterised by flow cytometry measuring the platelet activation marker CD62P and binding of fibrinogen to platelets as well as the formation of heterotypic platelet-leukocyte conjugates. RESULTS: Compared with saline, HES 130/0.4 dose-dependently impaired formation and firmness of the fibrin clot but did not affect the fibrin crosslinking activity of FXIIIa. At 40% but not at 10% haemodilution rate, HES 200/0.5 also increased platelet fibrinogen binding and both HES solutions increased expression of CD62P, the main receptor for platelet-leukocyte adhesion. HES 130/0.4 but not HES 200/0.5 increased formation of platelet-neutrophil conjugates and, to a lesser degree, platelet-monocyte conjugates. CONCLUSIONS: Our data demonstrate that HES 130/0.4 has similar adverse effects as HES 200/0.5. In particular, both types of HES impair coagulation capacity and stimulate, rather than attenuate, pro-inflammatory platelet function.
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spelling pubmed-28119522010-01-28 HES 130/0.4 impairs haemostasis and stimulates pro-inflammatory blood platelet function Sossdorf, Maik Marx, Sascha Schaarschmidt, Barbara Otto, Gordon P Claus, Ralf A Reinhart, Konrad Hartog, Christiane S Lösche, Wolfgang Crit Care Research INTRODUCTION: Hydroxyethyl starch (HES) solutions are widely used for volume replacement therapy but are also known to compromise coagulation, impair renal function and increase long-term mortality. To test the hypotheses that HES 130/0.4 has fewer adverse effects than HES 200/0.5 and exerts anti-inflammatory properties, we compared the effects of HES 130/0.4, HES 200/0.5 and saline on in vitro haemostasis and pro-inflammatory platelet function. METHODS: Whole blood samples from healthy volunteers were mixed with 6% HES 130/0.4, 10% HES 200/0.5, or normal saline to achieve a final haemodilution rate of 10% or 40%. Haemostatic capacity was characterised by thromboelastography (ROTEM) and measurement for FXIIIa activity. Platelet activation and pro-inflammatory platelet functions were characterised by flow cytometry measuring the platelet activation marker CD62P and binding of fibrinogen to platelets as well as the formation of heterotypic platelet-leukocyte conjugates. RESULTS: Compared with saline, HES 130/0.4 dose-dependently impaired formation and firmness of the fibrin clot but did not affect the fibrin crosslinking activity of FXIIIa. At 40% but not at 10% haemodilution rate, HES 200/0.5 also increased platelet fibrinogen binding and both HES solutions increased expression of CD62P, the main receptor for platelet-leukocyte adhesion. HES 130/0.4 but not HES 200/0.5 increased formation of platelet-neutrophil conjugates and, to a lesser degree, platelet-monocyte conjugates. CONCLUSIONS: Our data demonstrate that HES 130/0.4 has similar adverse effects as HES 200/0.5. In particular, both types of HES impair coagulation capacity and stimulate, rather than attenuate, pro-inflammatory platelet function. BioMed Central 2009 2009-12-22 /pmc/articles/PMC2811952/ /pubmed/20028511 http://dx.doi.org/10.1186/cc8223 Text en Copyright ©2009 Sossdorf et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research
Sossdorf, Maik
Marx, Sascha
Schaarschmidt, Barbara
Otto, Gordon P
Claus, Ralf A
Reinhart, Konrad
Hartog, Christiane S
Lösche, Wolfgang
HES 130/0.4 impairs haemostasis and stimulates pro-inflammatory blood platelet function
title HES 130/0.4 impairs haemostasis and stimulates pro-inflammatory blood platelet function
title_full HES 130/0.4 impairs haemostasis and stimulates pro-inflammatory blood platelet function
title_fullStr HES 130/0.4 impairs haemostasis and stimulates pro-inflammatory blood platelet function
title_full_unstemmed HES 130/0.4 impairs haemostasis and stimulates pro-inflammatory blood platelet function
title_short HES 130/0.4 impairs haemostasis and stimulates pro-inflammatory blood platelet function
title_sort hes 130/0.4 impairs haemostasis and stimulates pro-inflammatory blood platelet function
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2811952/
https://www.ncbi.nlm.nih.gov/pubmed/20028511
http://dx.doi.org/10.1186/cc8223
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