Examining platelet-fibrin interactions during traumatic shock in a swine model using platelet contractile force and clot elastic modulus.
Examining platelet-fibrin interactions during traumatic shock in a swine model using platelet contractile force and clot elastic modulus.
复制标题
使用血小板收缩力和凝块弹性模量检查猪模型创伤性休克期间血小板-纤维蛋白的相互作用。
DOI：
10.1097/mbc.0b013e3283456c68
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发表时间：
2011
期刊：
影响因子：
--
通讯作者：
Ward,KevinR
中科院分区：
文献类型：
--
作者：
White,NathanJ;Martin,ErikaJ;Brophy,DonaldF;Ward,KevinR
相当比例的严重损伤患者发展为早期凝血病，其特征在于异常凝块形成，这损害复苏并增加死亡率。我们以前已经证明了一个孤立的血栓弹力图在猪模型的非复苏创伤性休克的凝块强度下降。为了更仔细地检查在这种情况下的血小板-纤维蛋白相互作用，我们使用止血分析系统（HAS）（Hemodyne Inc.，美国弗吉尼亚州里士满）。在损伤前的基线和由氧债定义的创伤性休克的预定水平下，对全血进行采样用于HAS测量、代谢测量、细胞计数和纤维蛋白原浓度。雄性猪（N= 17）接受股骨骨折并控制动脉出血以实现80 ml/kg的氧债。休克期间血小板计数无变化，但纤维蛋白原浓度显著降低（167.6 vs. 66.7 mg/dl，P= 0.0007）。血栓形成过程中产生的血小板收缩力在休克期间没有改变（11.7 vs.10.4kdynes，P= 0.41），但血栓弹性模量动态改变，导致最终值较低（22.9 vs.17.3kdynes/cm 2，P< 0.0001）。在这个创伤性休克模型中，血小板功能得以保留，而终末凝块弹性模量在休克期间以与发育中的纤维蛋白纤维网络的机械性质的早期变化最一致的方式降低。
A significant proportion of severely injured patients develop early coagulopathy, characterized by abnormal clot formation, which impairs resuscitation and increases mortality. We have previously demonstrated an isolated decrease in clot strength by thrombelastography in a swine model of nonresuscitated traumatic shock. In order to more closely examine platelet–fibrin interactions in this setting, we define the observed decrease in clot strength in terms of platelet-induced clot contraction and clot elastic modulus using the Hemostasis Analysis System (HAS)(Hemodyne Inc., Richmond, Virginia, USA). Whole blood was sampled for HAS measurements, metabolic measurements, cell counts, and fibrinogen concentration at baseline prior to injury and again at a predetermined level of traumatic shock defined by oxygen debt. Male swine (N= 17) received femur fracture and controlled arterial hemorrhage to achieve an oxygen debt of 80 ml/kg. Platelet counts were unchanged, but fibrinogen concentration was reduced significantly during shock (167.6 vs. 66.7 mg/dl, P= 0.0007). Platelet contractile force generated during clot formation did not change during shock (11.7 vs. 10.4 kdynes, P= 0.41), but clot elastic modulus was dynamically altered, resulting in a lower final value (22.9 vs. 17.3 kdynes/cm 2, P< 0.0001). In this model of traumatic shock, platelet function was preserved, whereas terminal clot elastic modulus was reduced during shock in a manner most consistent with early changes in the mechanical properties of the developing fibrin fiber network.