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J Trauma. 2004 Jul;57(1 Suppl):S13-21.

Mechanisms of poly-N-acetyl glucosamine polymer-mediated hemostasis: platelet interactions.

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Department Surgery, VA Boston Healthcare System, Brigham and Women's Hospital, Harvard Medical Schools, Boston, MA, USA.



Investigations were performed to determine whether poly-N-acetyl glucosamine (p-GlcNAc) induces hemostasis by the activation of platelets.


Platelets were isolated from human blood, fixed in the presence poly-N-acetyl glucosamine fibers, and visualized with scanning electron microscopy. Platelet activation surface markers were measured by fluorescence multiphoton microscopy. Platelet aggregation in the presence of p-GlcNAc fibers and integrin receptor blockers was measured.


Scanning electron microscopy indicated that contact of platelets with poly-N-acetyl glucosamine fibers resulted in platelet activation. Fluorescent microscopy showed that contact of platelets with the marine polymer increased intracellular levels of free calcium and resulted in surface exposure of platelet phosphatidylserine, P selectin, and the alphaIIbbeta3 integrin. Antibody inhibitors of the platelet alphaIIbbeta3 integrin inhibited p-GlcNAc to stimulate fibrin polymerization.


Poly-N-acetyl glucosamine fiber material promotes hemostasis by the activation of platelets.

[Indexed for MEDLINE]

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