氨酸阻断了内毒素诱导的凝血激活
T Pernerstorfer1, U Hollenstein, J Hansen
1Department of Clinical Pharmacology-The Adhesion Research Group Elaborating Therapeutics (TARGET), University of Tromsø, Norway. thomas.pernerstorfer@univie.ac.at
Circulation
|December 22, 1999
概括
在人体内毒性模型中,未分离的氨酸 (UFH) 和低分子量氨酸 (LMWH) 有效地降低了由脂聚糖 (LPS) 触发的凝血激活. 这两种抗凝剂都抑制了血栓生成和上游/下游凝血因子激活.
科学领域:
- 凝血科学是一门凝血科学.
- 药理学 药理学是指药理学的学科.
- 败血症的研究研究.
背景情况:
- 脂聚糖 (LPS) 通过组织因子 (TF) /因子VIIa通路触发败血症诱导的散布性血管内凝血 (DIC).
- 抗凝剂在LPS诱导的凝血中的临床使用仍然未得到充分探索.
- 这项研究研究了UFH和LMWH对LPS诱导的凝血的影响.
研究的目的:
- 为了比较未分离氨酸 (UFH) 和低分子量氨酸 (LMWH) 与安慰剂的影响.
- 在实验性LPS诱导凝血模型中评估抗凝血功效.
- 评估抑制血栓生成和凝血因子激活.
主要方法:
- 在30名健康男性志愿者中进行随机,双盲,安慰剂对照试验.
- 给药LPS (2 ng/kg IV) 接下来是UFH,LMWH或安慰剂输注.
- 测量前热血素片段F(1+2),血栓前体蛋白 (TpP),TF阳性单细胞,激活因子VII和TF通路抑制剂水平.
主要成果:
- 而安慰剂组的F(1+2) 和TTP显著增加;TF阳性单细胞增加了一倍.
- UFH和LMWH显著降低了F(1+2) 和TTP水平.
- 两种肝素都降低了单细胞上的TF表达,增加了TF通路抑制剂,并降低了VIIa因子水平.
结论:
- 在早期的实验中,UFH和LMWH在LPS诱导的凝血中显示出抗凝血功效.
- 观察到成功抑制了血栓生成.
- 肝素对血凝因子在血栓的上游和下游的凸激活.
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