目的 探讨凝血异常在脓毒症并发急性肺损伤(ALI)发病中的作用.方法 采用盲肠结扎穿孔(CLP)制备小鼠脓毒症ALI模型,随机分为对照组、假手术组和造模组,不同时间点(2、4、8、12 h)观察肺组织损伤的病理和凝血指标;同时,采用ELISA检测血浆组织因子(TF)浓度的变化.结果 盲肠结扎穿孔12 h 后,肺组织出现明显炎症细胞浸润、蛋白渗出和毛细血管内弥漫血栓形成;与正常组和手术组比较,造模组凝血酶原时间(PT)、凝血酶时间(TT)、活化部分凝血酶时间(APTT)和D-二聚体(DD)显著升高(P<0.05),而纤维蛋白原(Fb)和血小板(Plt)计数显著降低(P<0.05).动态观察TF浓度,造模组TF浓度呈进行性升高,各组比较差异有统计学意义(P<0.05).结论 CLP可成功制备小鼠脓毒症ALI模型,凝血亢进与肺组织全身弥散性血管内凝血(DIC)参与脓毒症ALI的发病;TF是启动凝血异常的关键因素.%Objective To investigate the effects of coagulation dysfunction on sepsis - induced acute lung injury ( ALI ). Methods Mouse sepsis models were established by cecal ligation and puncture ( CLP ) and randomly divided into three groups: blank group, sham operation group and model group. Pathological changes of the lung tissues and coagulation markers were recorded at 2, 4, 8 and 12 hour. Meanwhile, blood concentration of TF was detected using enzyme - linked immunosorbent assay ( ELISA ). Results Observably inflammatory cell infiltration, exudation of fibrin and disseminated intravascular coagulation ( DIC ) were revealed in lung tissues 12 hours after CLP. The concentrations of PT, TT, APTT and DD were significantly increased, while Fbg and PLT significantly reduced, in model group, when compared with those in control group and sham operation group ( P < 0. 05 ). The concentrations of TF continually increased after CLP, with significant differences among the 3 groups ( P <0. 05 ). Conclusion Acute lung injury ( ALI ) model is successfully established using CLP. Coagulation activation and DIC in lung tissues participate in sepsis - induced ALI. TF is a key factor of the initiation of coagulopathy.
展开▼
