The antiplatelet activity of Escherichia coli lipopolysaccharide is mediated through a nitric oxide/cyclic GMP pathway

Joen Rong Sheu, W. C. Hung, Ching-Hua Su, C. H. Lin, L. W. Lee, Y. M. Lee, M. H. Yen

研究成果: 雜誌貢獻文章

23 引文 斯高帕斯(Scopus)


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 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/1), 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.
頁(從 - 到)317-326
期刊European Journal of Haematology
出版狀態已發佈 - 1999


ASJC Scopus subject areas

  • Hematology