Effects of N-acetyl glucosamine on platelet aggregation

N-acetyl glucosamine (NAG) alone did not aggregate platelets but in low concentrations shortened the delay phase of the $\text{Staphylococcus aureus}$ induced platelet aggregation in a concentration dependent manner, which suggests that NAG may be one of the components of the $\text{S. aureus}$ cell wall responsible for platelet aggregation. NAG, on the other hand, inhibited collagen induced platelet aggregation and the secondary platelet aggregation induced by epinephrine and ADP. This inhibition appears to be due to impurities that occur at higher levels in some NAG lots than in others. NAG has also been shown to decrease the length of time before the release of ATP from platelets when $\text{S. aureus}$ is the aggregating agent.