硫化氢对组织因子诱导的弥散性血管内凝血家兔体外凝血活性的影响

Effects of hydrogen sulfide on in vitro coagulation activity in rabbits with tissue factor-induced DIC

目的探讨硫化氢对组织因子诱导的弥散性血管内凝血(DIC)家兔凝血活性的影响。方法健康青紫蓝家兔通过静脉注射组织因子复制DIC模型。采用全自动凝血分析仪检测活化部分凝血活酶时间(APTT)和凝血酶原时间(PT);凝聚法检测血浆纤维蛋白(原)降解产物(FDP)。结果注射组织因子至5 min时,APTT和PT较注射前缩短(P<0.05),15、45 min时,APTT和PT较注射前延长(P<0.05),注射组织因子后的血样品,FDP检测均出现乳胶颗粒凝集;经硫化氢处理,注射组织因子前血浆PT无明显变化,中、高剂量组APTT延长(P<0.05),FDP检测未出现乳胶颗粒凝集;注射组织因子5 min时,中、高剂量组PT较对照组延长(P<0.05),高剂量组APTT较对照组延长(P<0.05);15、45 min时,PT仅在高剂量时较对照组延长(P<0.05),APTT在中、高剂量时较对照组均延长(P<0.05);FDP检测,5和15 min时中、高剂量组的乳胶颗粒凝集较对照组明显减弱,45 min时,各组的乳胶颗粒凝集均不明显。结论硫化氢对实验性DIC动物体外凝血有一定的抑制作用。

Objective To explore the effects of sodium sulfide on in vitro coagulation in rabbits with tissue factor-induced disseminted intravascular coagulation（ DIC）. Methods DIC model was prepared by intravenous injection of tissue factor（ TF）. Every plasma was assigned into sodium sulfide（ treated with 25,50,100 μg / ml sodium bisulfide）,normal saline and control groups. Prothrombin time（ PT）,activated partial thromboplastin time（ APTT）,and fibrin degradation products（ FDP） were determined. Results At 5 min of injection： PT in rabbits treated with sodium bisulfide and APTT in high dose group were significantly prolonged（ P 0. 01,P 0. 05）,FDP agglutination was abated in middle and high dose groups; at 15 and 45 min,PT in high dose and APTT in middle and high dose group were prolonged（ P 0. 05,P 0. 01）,FDP agglutination was abated in middle and high dose groups. When compared with the prior injection of tissue factor,5 min： PT in control and negative groups,and APTT in all groups were shortened（ P 0. 05,P 0. 01）,FDP agglutination was enhanced in all groups;at 15 min,there was not any difference in PT among all groups,APTT was prolonged in all groups（ P 0. 05）,FDP agglutination was prolonged in all groups; at 45 min,PT and APTT were prolonged in all groups（ P 0. 05,P 0. 01）,FDP agglutination was little. Conclusions Hydrogen sulfide inhibits in vitro coagulation activity in rabbits with TF-induced DIC by its inhibitor to activating coagulation factor.