摘要
本研究探讨急性减压病时机体凝血纤溶系统的变化规律及机制。建立以新西兰大白兔为模型的急性减压病动物模型,观察该模型在加压前、减压后的生存率及减压病症状。在加压前及减压后0、3、24小时抽取动脉血,以胶乳凝集半定量法动态测定凝血酶原时间(prothrombin time,PT)、活化部分凝血活酶时间(activated partial thromboplas-tin time,APTT)、凝血酶原时间(thrombin time,TT)、纤维蛋白原(fibrinogan,Fib)、纤维蛋白原降解产物(fibrinogendegradation product,FDP)、D-二聚体的数值;ELISA法测定各个时间点实验兔血浆中的纤维蛋白肽A(fibrinopeptideA,FPA)、纤溶酶-抗纤溶酶复合物(plasmin-antiplasmin complex,PAP)、纤溶酶原激活物抑制因子1(plasminogen acti-vator inhibitor-1,PAI-1)的动态变化。ELISA法测定不安全减压后血栓调节蛋白(thrombomodulin,TM)的变化。结果显示:成功建立急性减压病兔模型;减压后15分钟即出现血浆APTT、TT延长,Fib含量增高,减压后3小时尤为显著,24小时较前恢复,但有明显减压病症状者24小时后仍存在显著改变;血浆FDP含量在减压后3小时显著降低;有明显减压病症状者在减压后24小时D-二聚体显著增高。ELISA测定显示,FPA在减压后15分钟明显增高,与加压前相比有显著差异(p<0.05),24小时恢复至接近基值;PAP在减压后呈现升高趋势,但与加压前相比无统计学差异。PAI-1低于检测值,未检出。TM在减压后明显升高,加压前为0.12±0.03μg/ml,减压后15分钟为0.42±0.15μg/ml,两者相比较有显著差异(p=0.035)。结论急性减压病时机体的凝血纤溶系统出现显著变化,表现为凝血时间的延长、纤溶系统的激活,呈动态变化。血管内皮损伤可能是导致急性减压病时机体凝血纤溶系统变化的机制之一。
This study was purposed to investigate the changes in coagulation and fibrinolysis pathways in rabbits suffered from the acute decompression sickness (DCS). Model of DCS in rabbits was established. Survival rate and symptoms of DCS in animal model was monitored. The prothrombin time ( PT), activated partial thromboplastin time (APTT), thrombin time (TT), fibrinogen (Fib), fibrinogen degradation product (FDP) and D-dimers were measured before compression and at 0, 3, 24 hours after decompression by latex agglutination semiquantitative methods. The changes of plasmin-antiplasmin complex ( PAP), fibrinopeptide A ( FPA ), plasminogen activator inhibitor 1 ( PAI-1 ) and thrombomodulin(TM) were measured by ELISA at different time points after decompression. The results showed that the model of DCS in rabbits was successfully established. There was a statistically significant extension in APTT, "FF, increase of Fib concentration at 15 minutes after decompression, the changes were peaked at 3 hours and recovered at 24 hours after decompression. The concentration of FDP significantly decreased at 3 hours after decompression. The concentration of D-dimers significantly increased at 24 hours after decompression in rabbits model with DCS. FPA concentration was significantly increased at 15 minutes and recovered at 24 hours after decompression. PAP concentration was increased after decompression, but had no significant changes. PAI-1 could not be detected. TM significantly increased after decompression. It is concluded that the acute DCS significantly impacts on blood coagulation system in rabbit model. It is shown that hypocoagulation occurred at initial time and hyperfibdnolysis subsequently, which varied with time. The damage of blood vessel endotheliurn may be one of the causes of these variations.
出处
《中国实验血液学杂志》
CAS
CSCD
2010年第1期191-194,共4页
Journal of Experimental Hematology
基金
总后司令部科研课题资助项目(编号07-3301)
关键词
急性减压病
凝血
纤溶
血管内皮
decompression gickness
coagulation
fibrinolysis
blood vessel endothelium