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The antiplatelet activity of Escherichia coli lipopolysaccharide is mediated through a nitric oxide/cyclic GMP pathway
Author(s) -
Sheu J. R.,
Hung W. C.,
Su C. H.,
Lin C. H.,
Lee L. W.,
Lee Y. M.,
Yen M. H.
Publication year - 1999
Publication title -
european journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0902-4441
DOI - 10.1111/j.1600-0609.1999.tb01909.x
Subject(s) - platelet , nitric oxide , lipopolysaccharide , activator (genetics) , chemistry , platelet activation , intracellular , escherichia coli , platelet activating factor , pharmacology , biochemistry , endocrinology , medicine , receptor , organic chemistry , gene
In this study, Escherichia coli LPS dose‐dependently (100–500 μg/ml) and time‐dependently (10–60 min) inhibited platelet aggregation in human and rabbit platelets stimulated by agonists. LPS also dose‐dependently inhibited the intracellular Ca 2+ mobilization in human platelets stimulated by collagen. In addition, LPS (200 and 500 μg/ml) significantly increased the formation of cyclic GMP but not cyclic AMP in platelets. LPS (200 μg/ml) significantly increased the production of nitrate within a 10‐min incubation period. Furthermore, LPS also dose‐dependently inhibited platelet aggregation induced by PDBu (30 nmol/l), a protein kinase C activator. These results indicate that the antiplatelet activity of E. coli LPS may be involved in the activation of a nitric oxide/cyclic GMP pathway in platelets, resulting in inhibition of platelet aggregation. Therefore, LPS‐mediated alteration of platelet function may contribute to bleeding diathesis in septicemic and endotoxemic patients.