Jr. Sheu et al., The antiplatelet activity of Escherichia coli lipopolysaccharide is mediated through a nitric oxide cyclic GMP pathway, EUR J HAEMA, 62(5), 1999, pp. 317-326
In this study, Escherichia coli LPS dose-dependently (100-500 mu g/ mi) and
time-dependently (10-60 min) inhibited platelet aggregation in human and r
abbit platelets stimulated by agonists. LPS also dose-dependently inhibited
the intracellular Ca2+ mobilization in human platelets stimulated by colla
gen. In addition, LPS (200 and 500 mu g/ml) significantly increased the for
mation of cyclic GMP but not cyclic AMP in platelets. LPS (200 mu g/ml) sig
nificantly increased the production of nitrate within a 10-min incubation p
eriod. Furthermore, LPS also dose-dependently inhibited platelet aggregatio
n 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 t
he activation of a nitric oxide/cyclic GMP pathway in platelets, resulting
in inhibition of platelet aggregation. Therefore, LPS-mediated alteration o
f platelet function may contribute to bleeding diathesis in septicemic and
endotoxemic patients.