STRAIN ENHANCEMENT OF ELASTIC-MODULUS IN FINE FIBRIN CLOTS

STRAIN ENHANCEMENT OF ELASTIC-MODULUS IN FINE FIBRIN CLOTS
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DOI:
10.1016/0049-3848(88)90129-6
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发表时间:
1988-12-15
影响因子:
7.5
通讯作者:
FERRY, JD
FERRY, JD
中科院分区:
医学3区
文献类型:
--
作者:
BALE, MD;FERRY, JD

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在pH 8.5,离子强度0.45,原纤维侧向聚集最小的条件下制备纤维蛋白凝块,并通过因子XIIIA连接(交联),在恒定的静态剪切应变(γ)下进行。具有叠加的小的振荡应变。在振动变形中测得的增量剪切模数(动态储能模数)在小的静态应变(最高可达0.1)时与应变无关,且与静力模数大致相等。在较高的静态应变下,它迅速增加,在伽马时增加了5到8倍。=0.35。与早期未结扎血栓的数据比较表明,除了非常高的应变外,僵硬的增加与结扎无关。这种增强归因于网络纤维之间的额外强迫接触,因为线束被弯曲和定向。当静态应变维持到一天时,在用XIIIA因子结扎的凝块中,增强的增量弹性系数保持不变或略有下降,去除应力后,凝块几乎恢复到原来的形状。这与未结扎的血栓的行为形成对比,在未结扎的血栓中,随着增量弹性模量下降到其小应变值,大部分增强功能逐渐丧失,并且在去除应力后有大量永久变形。后一种行为被归因于高应变下网链的逐渐断裂,随后它们以宽松的配置重新连接,但留下了一些在休息状态下只能非常缓慢地恢复的结构损伤。结扎原纤维明显消除了断股的可能性。
Fine fibrin clots, prepared at pH 8.5, ionic strength 0.45, with minimal lateral aggregation of protofibrils, and ligated (cross-linked) by factor XIIIa, were subjected to constant static shear strain (.gamma.) with superposed small oscillating strains. The incremental shear modulus (dynamic storage modulus) measured in the oscillating deformations was strain-independent at small static strains (up to about 0.1) and approximately equal to the static modulus. At higher static strains, it increased rapidly, up by a factor of 5 to 8 at .gamma. = 0.35. Comparison with earlier data on unligated clots showed that the enhancement of stiffness was independent of ligation except at very high strains. The enhancement is attributed to additional forced contacts between network fibers as the strands are bent and oriented. When the static strain was maintained for up to one day, in a clot ligated by factor XIIIa the enhanced incremental modulus remained constant or decreased slightly, and after removal of stress the clot returned almost to its original shape. This contrasts with the behavior of unligated clots, where most of the enhancement was progressively lost as the incremental modulus fell toward its small-strain value, and there was a substantial permanent deformation after the removal of stress. The latter behavior has been attributed to gradual severance of network strands at high strains, followed by their rejoining in relaxed configurations, but leaving some structural damage that is only very slowly recovered in the resting state. Ligation of protofibrils evidently eliminates the possbility of strand rupture.