Zhang Jian-ning, Wood Jennifer, Bergeron Angela L, McBride Latresha, Ball Chalmette, Yu Qinghua, Pusiteri Anthony E, Holcomb John B, Dong Jing-fei
Section of Thrombosis Research, Department of Medicine, Baylor College of Medicine, Houston, Texas 77030, USA.
J Trauma. 2004 Aug;57(2):216-23. doi: 10.1097/01.ta.0000093366.98819.fe.
Hemorrhage is a major complication of trauma and often becomes more severe in hypothermic patients. Although it has been known that platelets are activated in the cold, studies have been focused on platelet behavior at 4 degrees C, which is far below temperatures encountered in hypothermic trauma patients. In contrast, how platelets function at temperatures that are commonly found in hypothermic trauma patients (32-37 degrees C) remains largely unknown, especially when they are exposed to significant changes in fluid shear stress that could occur in trauma patients due to hemorrhage, vascular dilation/constriction, and fluid resuscitation.
Using a cone-plate viscometer, we have examined platelet activation and aggregation in response to a wide range of fluid shear stresses at 24, 32, 35, and 37 degrees C.
We found that shear-induced platelet aggregation was significantly increased at 24, 32, and 35 degrees C as compared with 37 degrees C and the enhancement was observed in whole blood and platelet-rich plasma. In contrast to observation made at 4 degrees C, the increased shear-induced platelet aggregation at these temperatures was associated with minimal platelet activation as determined by the P-selectin expression on platelet surface. Blood viscosity was also increased at low temperature and the changes in viscosity correlated with levels of plasma total protein and fibrinogen.
We found that platelets are hyper-reactive to fluid shear stress at temperatures of 24, 32, and 35 degrees C as compared with at 37 degrees C. The hyperreactivity results in heightened aggregation through a platelet-activation independent mechanism. The enhanced platelet aggregation parallels with increased whole blood viscosity at these temperatures, suggesting that enhanced mechanical cross-linking may be responsible for the enhanced platelet aggregation.
出血是创伤的主要并发症，在体温过低的患者中往往会变得更加严重。虽然已知血小板在低温下会被激活，但研究主要集中在4℃时血小板的行为，而这一温度远低于体温过低的创伤患者所经历的温度。相比之下，血小板在体温过低的创伤患者常见的温度（32 - 37℃）下如何发挥功能仍 largely 未知，尤其是当它们暴露于创伤患者因出血、血管扩张/收缩和液体复苏而可能发生的显著流体剪切应力变化时。
我们使用锥板粘度计，检测了在24℃、32℃、35℃和37℃下，血小板对广泛范围的流体剪切应力的激活和聚集情况。
我们发现，与37℃相比，在24℃、32℃和35℃时，剪切诱导的血小板聚集显著增加，并且在全血和富含血小板的血浆中均观察到这种增强。与在4℃时的观察结果相反，在这些温度下，剪切诱导的血小板聚集增加与通过血小板表面P - 选择素表达所确定的最小血小板激活相关。低温时血液粘度也增加，并且粘度变化与血浆总蛋白和纤维蛋白原水平相关。
我们发现，与37℃相比，血小板在24℃、32℃和35℃时对流体剪切应力反应过度。这种反应过度通过一种不依赖血小板激活的机制导致聚集增强。在这些温度下，血小板聚集增强与全血粘度增加平行，表明增强的机械交联可能是血小板聚集增强的原因。
