Heinrich D, Görg T, Schulz M
Department of Internal Medicine, University Hospital, Justus Liebig University, Giessen, FRG.
Haemostasis. 1988;18 Suppl 3:48-54. doi: 10.1159/000215867.
Heparin-induced alterations of platelet function have repeatedly been reported over the last 30 years. The development of low-molecular-weight (LMW) heparin fractions prompted us to compare the effect of unfractionated (UF) heparin and LMW heparin on platelet function. Heparin was applied intravenously to healthy volunteers in a dose of 100 U (antifactor Xa)/kg body weight. Sequential evaluation of platelet function ex vivo confirmed that UF heparin may activate platelets in vivo. Studying the ADP-induced fibrinogen binding to platelets in vivo, we were able to show that the effect of heparin on platelets is antibody- and antithrombin-III-independent. LMW heparin fractions in general exhibit a reduced platelet activating activity although there are differences between the LMW heparin fractions available. The stimulating effect of LMW heparin on platelets disappears below a mean molecular weight of 3,000 daltons.
在过去30年里，肝素诱导的血小板功能改变已被多次报道。低分子量（LMW）肝素片段的出现促使我们比较普通肝素（UF）和LMW肝素对血小板功能的影响。将肝素以100 U（抗Xa因子）/千克体重的剂量静脉注射给健康志愿者。对体外血小板功能的连续评估证实，UF肝素可能在体内激活血小板。通过研究体内ADP诱导的纤维蛋白原与血小板的结合，我们能够证明肝素对血小板的作用不依赖抗体和抗凝血酶III。尽管现有的LMW肝素片段存在差异，但一般而言，LMW肝素片段的血小板激活活性降低。当平均分子量低于3000道尔顿时，LMW肝素对血小板的刺激作用消失。
