Key result
Escherichia coli LPS dose-dependently (100-500 microg/ml) and time-dependently (10-60 min) inhibited platelet aggregation in human and rabbit platelets via a nitric oxide/cyclic GMP pathway.
Population
Human and rabbit platelets
Design
Preclinical
Authors
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May explain sepsis-related bleeding; leaves open whether NO/cGMP modulation alters human outcomes.
E. coli LPS inhibits platelet aggregation via a nitric oxide/cyclic GMP pathway, which may contribute to bleeding diathesis in sepsis.
Sheu et al. (1999) studied this question. Escherichia coli lipopolysaccharide (LPS) was evaluated on platelet aggregation. Escherichia coli LPS dose-dependently (100-500 microg/ml) and time-dependently (10-60 min) inhibited platelet aggregation in human and rabbit platelets via a nitric oxide/cyclic GMP pathway.
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