Schousboe I, Rasmussen M S, Lintner R
Department of Medical Biochemistry, Panum Institute, University of Copenhagen, Denmark.
Blood Coagul Fibrinolysis. 1994 Aug;5(4):503-9.
In normal plasma, high molecular mass dextran sulphate (DS500) induces formation of amidolytic activity towards the chromogenic substrate H-D-Pro-Phe-Arg-p-nitroanilide (S-2302) specific to factor XII and kallikrein. No amidolytic activity was formed when plasma deficient in prekallikrein was exposed to DS500. In contrast, factor XII amidolytic activity was formed upon exposure to sulphatide or acidic phospholipids. To assess whether DS500 interferes with the sulphatide and the acidic phospholipid in activating factor XII, plasma deficient in prekallikrein was incubated with phosphatidylinositol phosphate (PtdInsP) and sulphatide at the conditions necessary for activation with these surfaces and various concentrations of DS500. DS500 inhibited both the PtdInsP and the sulphatide-mediated autoactivation in an antithrombin III independent manner. Heparin also inhibited the PtdInsP mediated autoactivation but not that mediated by sulphatide. The heparin inhibition was due to enhancement of the antithrombin III activity, which could be partly blocked by preincubation of plasma with rabbit anti-human antithrombin III IgG.
在正常血浆中，高分子质量硫酸葡聚糖（DS500）可诱导对凝血因子XII和激肽释放酶特异的生色底物H-D-脯氨酸-苯丙氨酸-精氨酸-对硝基苯胺（S-2302）产生酰胺水解活性。当将缺乏前激肽释放酶的血浆暴露于DS500时，未形成酰胺水解活性。相反，当暴露于硫脂或酸性磷脂时，会形成凝血因子XII酰胺水解活性。为了评估DS500是否在激活凝血因子XII时干扰硫脂和酸性磷脂，将缺乏前激肽释放酶的血浆与磷脂酰肌醇磷酸（PtdInsP）和硫脂在这些表面激活所需的条件以及不同浓度的DS500下孵育。DS500以抗凝血酶III非依赖性方式抑制PtdInsP和硫脂介导的自身激活。肝素也抑制PtdInsP介导的自身激活，但不抑制硫脂介导的自身激活。肝素的抑制作用是由于抗凝血酶III活性增强，用兔抗人抗凝血酶III IgG预孵育血浆可部分阻断这种增强作用。
