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
Sheu, J. R., Hung, W. C., Su, C-H., Lin, C. H., Lee, L. W., Lee, Y. M., & Yen, M. H. (1999). The antiplatelet activity of Escherichia coli lipopolysaccharide is mediated through a nitric oxide/cyclic GMP pathway. European Journal of Haematology, 62(5), 317-326.