失血性休克大鼠凝血因子的变化研究

本研究观察SD大鼠失血性休克过程中凝血因子的变化 ,探讨凝血连锁反应在休克发生、发展过程中的作用机制。制作大鼠失血性休克模型后 ,4 0只大鼠随机分为休克前组、休克 1、2、4、6、8、12和 2 4小时组。分别检测各组假血管性血友病因子 (vWF) ,凝血因子Ⅷ (FⅧ ) ,组织因子 (TF) ,D 二聚体 (D D) ,纤维蛋白原 (FIB)的血浆浓度及观察凝血酶原时间 (PT)、活化部分凝血酶原时间 (APTT)变化。结果表明 :与休克前比较 ,各休克组PT、APTT逐渐延长 ,于休克后 4 - 6小时显著延长 (P <0 .0 0 1) ,APTT平均 5 9.7秒 ,PT平均 30 .2秒。休克后 ,血浆D 二聚体显著增加 (P <0 .0 0 1) ,于休克 8小时达到峰值。血浆vWF、FⅧa、TF、FIB于休克早期增加 ,随着休克的发展 ,纤维蛋白原于休克 2小时开始明显下降 (P <0 .0 0 1) ,休克 12小时降至最低值。TF、vWF、FⅧa分别于休克 6小时、8小时开始明显下降 (P <0 .0 0 1或P <0 .0 5 )。凝血因子消耗比率 :FⅧ为 (86 .1± 1.8% ) ,纤维蛋白原为 (89.6± 0 .6 % ) ,假血管性血友病因子为 (5 5± 1.4 % ) ,组织因子为 (6 2± 2 .5 % ) ,其中 ,FⅧ、纤维蛋白原消耗比例较大。失血性休克时以外源性凝血途径激活为主 ,内源性凝血途径作用较小。纤维蛋白原和D 二聚体、PT、APTT可用

Study on Changes of Blood Coagulation Factors in Rats with Hemorrhagic Shock

The study was aimed to observe the changes of blood coagulation factors in the SD rats suffered from hemorrhagic shock, and to investigate the mechanism of coagulation cascade reaction in the course of shock. The model of hemorrhagic shock was established. 40 SD rats were randomized into eight groups: pre-shock, and 1, 2, 4, 6, 8, 12 and 24 hours after shock, and the levels of plasma FVIII, vWF, TF, D-dimer, FIB, APTT and PT were detected respectively. The result showed that APTT and PT were gradually prolonged, which were significant within 4-6 hour after shock (P < 0.05). APTT and PT were 59.7 seconds and 30.2 seconds respectively. The level of plasma D-dimer markedly increased, and peaked at 8 hour after shock. The level of fibrinogen, TF, vWF and FVIIIa increased in the initial stage of shock. With the development of shock, fibrinogen markedly reduced from 2nd hour (P < 0.05) and dropped to the minimum at 7 hours after shock. Plasma TF, vWF, FVIII significantly decreased after 6 hours and 8 hours (P < 0.001). The ratios of the consumed coagulation factors: FVIII of (86.1 +/- 1.8)%, fibrinogen of (89.6 +/- 0.6)%, vWF (55 +/- 1.4)%, TF (62 +/- 2.5)%. Thus, coagulation factor I (fibrinogen) and FVIII were preferentially consumed. The extrinsic coagulation pathway was dominantly activated, whereas the intrinsic coagulation pathway played a less important role. Fibrinogen and D-dimer might be valuable for the prognosis of patients suffered from shock. It is concluded that hemorrhagic shock trigger the coagulation cascade reaction, and the coagulation factors are greatly consumed. Unbalance of coagulation system plays an important role in the progress of shock.