Extensive studies revealed the role of blood lipid microparticles (liposomes, microvesicles) in activation of coagulation cascade. The direct interaction of fibrinogen/fibrin with lipid surfaces and its consequence for hemostasis received much less attention. We observed pronounced changes in both clot morphology and kinetics of fibrin clotting in the presence of artificial liposomes. The evidence was obtained that lipid microparticles per se present a diffusion barrier to the three-dimensional fibril assembling and pose spatial restrictions for fiber elongation. On the other hand, fibrinogen adsorption results in its high local concentration on liposome surface that accelerates fibrin polymerization. Adsorption induces Fg secondary structure alterations which may contribute to the abnormal clot morphology. In dependence on lipid composition and size of microparticles, the interplay of all the outlined mechanisms determines functionally important changes of clot morphology. The obtained results contribute to the knowledge of clotting mechanisms in the presence of artificial and natural lipid microparticles.

广泛的研究揭示了血脂微粒（脂质体，微囊泡）在凝血级联反应的激活中的作用。纤维蛋白原/纤维蛋白与脂质表面的直接相互作用及其止血作用受到的关注较少。我们观察到在存在人工脂质体的情况下，血凝块形态和血纤蛋白凝结动力学均发生了明显变化。获得的证据表明，脂质微粒本身对三维纤维的组装提出了扩散障碍，并为纤维伸长带来了空间限制。另一方面，血纤蛋白原的吸附导致其在脂质体表面上的高局部浓度，从而加速了血纤蛋白的聚合。吸附引起Fg二级结构的改变，这可能会导致血凝块形态异常。根据脂质的组成和微粒的大小，所有概述机制的相互作用决定了血凝块形态在功能上的重要变化。所获得的结果有助于在存在人工和天然脂质微粒的情况下了解凝血机理。