Schramko A A, Kuitunen A H, Suojaranta-Ylinen R T, Niemi T T
Department of Anaesthesiology and Intensive Care Medicine, Helsinki University Central Hospital, Helsinki, Finland.
Acta Anaesthesiol Scand. 2009 Jul;53(6):731-5. doi: 10.1111/j.1399-6576.2008.01901.x. Epub 2009 Feb 23.
Gelatin solution impairs coagulation. The mechanism of coagulopathy is incompletely defined. The purpose of this study was to evaluate the capacity of single coagulation factors to reverse gelatin-promoted whole-blood coagulation disorders in vitro.
Venous blood was withdrawn from 12 volunteers in a crossover study. Four percent succinylated gelatin was added to citrated whole-blood samples to make a 40 vol% end-concentration of gelatin. The baseline and 40 vol% samples, and samples with addition of fresh-frozen plasma (FFP), fibrinogen, coagulation factors XIII (FXIII) or VIII, together with the von Willebrand factor (FVIII+vWF), were analysed by thromboelastometry (ROTEM. Coagulation was initiated by tissue thromboplastin (ExTEM with and without cytochalasin to determine the functional component of fibrinogen (FibTEM.
Initiation of coagulation and fibrin formation were delayed at 40 vol% gelatin dilution. At this stage, the median (25th-75th percentiles) maximum clot firmness (MCF) was 76.3 (65.9-80.0) and 32.5 (27.4-45.0)% of the pre-dilution value in ExTEM and FibTEM thromboelastometry, respectively. Coagulation time was corrected by addition of fibrinogen and FFP in ExTEM and FibTEM analysis, whereas FVIII or FXIII had minimal effects. MCF was partly restored only by FFP in ExTEM. In FibTEM analysis, MCF improved more by fibrinogen than by FVIII+VWF, FXIII or FFP.
Gelatin-induced whole-blood coagulation disorder in vitro is mainly dependent on the initial fibrinogen-fibrin interaction. The proposed mechanism might suggest not to reverse gelatin coagulopathy solely by fibrinogen administration. The administration of FFP, a mixture of different coagulation factors, reversed the gelatin-induced in vitro coagulopathy the best.
明胶溶液会损害凝血功能。凝血病的机制尚未完全明确。本研究的目的是评估单一凝血因子在体外逆转明胶促进的全血凝血障碍的能力。
在一项交叉研究中，从12名志愿者身上采集静脉血。将4%的琥珀酰明胶添加到枸橼酸化全血样本中，使明胶的终浓度达到40体积%。通过血栓弹力图（ROTEM）分析基线样本、40体积%的样本，以及添加新鲜冰冻血浆（FFP）、纤维蛋白原、凝血因子 XIII（FXIII）或 VIII 以及血管性血友病因子（FVIII + vWF）的样本。通过组织凝血活酶启动凝血（有或没有细胞松弛素的ExTEM，以确定纤维蛋白原的功能成分（FibTEM）。
在40体积%明胶稀释时，凝血启动和纤维蛋白形成延迟。在此阶段，在ExTEM和FibTEM血栓弹力图中，最大血凝块硬度（MCF）的中位数（第25 - 75百分位数）分别为稀释前值的76.3（65.9 - 80.0）%和32.5（27.4 - 45.0）%。在ExTEM和FibTEM分析中，添加纤维蛋白原和FFP可纠正凝血时间，而FVIII或FXIII的作用最小。在ExTEM中，只有FFP能部分恢复MCF。在FibTEM分析中，纤维蛋白原比FVIII + VWF、FXIII或FFP更能改善MCF。
体外明胶诱导的全血凝血障碍主要取决于最初的纤维蛋白原 - 纤维蛋白相互作用。所提出的机制可能表明不应仅通过给予纤维蛋白原来逆转明胶凝血病。给予FFP（一种不同凝血因子的混合物）能最好地逆转体外明胶诱导的凝血病。
