Structural origins of fibrin clot rheology

Structural origins of fibrin clot rheology
复制标题

DOI:
10.1016/s0006-3495(99)77113-4
复制
发表时间:
1999-11-01
影响因子:
3.4
通讯作者:
Lorand, L
Lorand, L
中科院分区:
生物学3区
文献类型:
--
作者:
Ryan, EA;Mockros, LF;Lorand, L

文献摘要

被引文献

相似文献

在纤维蛋白凝块中研究了与网络形态和因子XIIIa诱导的交联相关的凝块流变学行为的起源。通过改变纤维蛋白原、凝血酶和钙离子的浓度来操纵网络形态,并且通过FXIIIa的合成活性中心抑制剂来控制交联。网络功能(纤维长度,纤维直径,纤维和分支密度)的定量测量进行了分析,从立体对扫描电子显微镜照片构建的计算机化三维模型。大的纤维直径和长度,只有当分支是最小的,纤维长度的增加通常与纤维直径的增加。三条纤维连接的连接点是主要的分支点类型。用流变仪测量凝块的粘弹性,并与网络的结构特征相关联。在纤维蛋白原恒定但凝血酶和钙浓度变化的情况下,样品(交联和非交联)的刚度达到最大,表现出大纤维尺寸和大分支之间的平衡。凝块硬度也增强了纤维和分支点密度在更大的纤维蛋白原浓度。FXIIIa催化的交联反应仅最小程度地改变了网络形态,这似乎是:最有可能通过现有纤维的硬化来增加凝块硬度。
The origins of clot rheological behavior associated with network morphology and factor XIIIa-induced crosslinking were studied in fibrin clots. Network morphology was manipulated by varying the concentrations of fibrinogen, thrombin, and calcium ion, and cross-linking was controlled by a synthetic, active-center inhibitor of FXIIIa. Quantitative measurements of network features (fiber lengths, fiber diameters, and fiber and branching densities) were made by analyzing computerized three-dimensional models constructed from stereo pairs of scanning electron micrographs. Large fiber diameters and lengths were established only when branching was minimal, and increases in fiber length were generally associated with increases in fiber diameter. Junctions at which three fibers joined were the dominant branchpoint type. Viscoelastic properties of the clots were measured with a rheometer and were correlated with structural features of the networks. At constant fibrinogen but varying thrombin and calcium concentrations, maximal rigidities were established in samples (both cross-linked and noncross-linked) which displayed a balance between large fiber sizes and great branching. Clot rigidity was also enhanced by increasing fiber and branchpoint densities at greater fibrinogen concentrations. Network morphology is only minimally altered by the FXIIIa-catalyzed cross-linking reaction, which seems to:augment clot rigidity most likely by the stiffening of existing fibers.