Thatte Hemant S, Zagarins Sofija, Khuri Shukri F, Fischer Thomas H
Department Surgery, VA Boston Healthcare System, Brigham and Women's Hospital, Harvard Medical Schools, Boston, MA, USA.
J Trauma. 2004 Jul;57(1 Suppl):S13-21. doi: 10.1097/01.ta.0000136743.12440.89.
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.
开展研究以确定聚-N-乙酰葡糖胺（p-GlcNAc）是否通过激活血小板来诱导止血。
从人血中分离血小板，在聚-N-乙酰葡糖胺纤维存在的情况下进行固定，并用扫描电子显微镜观察。通过荧光多光子显微镜测量血小板活化表面标志物。测量在p-GlcNAc纤维和整合素受体阻滞剂存在下的血小板聚集情况。
扫描电子显微镜显示血小板与聚-N-乙酰葡糖胺纤维接触导致血小板活化。荧光显微镜显示血小板与海洋聚合物接触会增加细胞内游离钙水平，并导致血小板磷脂酰丝氨酸、P选择素和αIIbβ3整合素的表面暴露。血小板αIIbβ3整合素的抗体抑制剂抑制p-GlcNAc刺激纤维蛋白聚合。
聚-N-乙酰葡糖胺纤维材料通过激活血小板促进止血。
