低压低氧性肺动脉高压中组织因子致高凝状态的研究  

Tissue Factor Triggers Hypercoagulable State in Hypobaric Hypoxia-induced Pulmonary Hypertension

作　　者：赵晟[1] 姚小燕[1] 薛新颖[1] 高培良[1] 邓会[1] 张婧媛[1] 潘磊[1] 王勇[1] 

机构地区：[1]首都医科大学附属北京世纪坛医院呼吸与危重症医学科低氧实验室,北京市100038

出　　处：《中国分子心脏病学杂志》2016年第6期1920-1922,共3页Molecular Cardiology of China

摘　　要：目的观察低压低氧性肺动脉高压高凝状态中组织因子(TF)的作用。方法将16只健康雄性SD大鼠随机分为实验组和对照组,每组各8只。实验组大鼠置于全自动调节低压低氧舱内,持续暴露于模拟低压低氧环境(气压50k Pa,氧浓度10%);对照组大鼠置于同室,暴露于常压常氧环境。4周后采用右心导管检查测定各组大鼠平均肺动脉压(m PAP);用电子天平称量右心室(RV)、左心室(LV)、室间隔(S)重量,以RV/(LV+S)计右心肥厚指数(RVHI);行苏木精-伊红(HE)染色,观察肺组织显微形态学;ELISA测定血浆HIF-1α、VEGF、TF浓度。结果与对照组相比,实验组大鼠的m PAP、RVHI均显著高于对照组(P<0.05);实验组大鼠肺组织可见典型肺血管重塑,肺动脉中可见多发附壁血栓形成;实验组大鼠血浆HIF-1α、VEGF、TF表显著达升高(P<0.05)。结论低压低氧性肺动脉高压中TF的异常表达与肺血栓形成及高凝状态相关,外源性凝血途径可能在高凝机制中起到重要作用。Objective To This study aims to investigate the potential role of tissue factor（TF） in hypercoagulable state of hypobaric hypoxia-induced pulmonary. Methods 16 healthy male SD rats were randomly divided into experiment group and control group, 8 for each group. The experiment group was continuously housed in an automatic adjusting hypobaric hypoxia chamber（atmospheric pressure of about 50 k Pa, oxygen concentration 10%）, the control group is housed under normobaric normoxic condition in the same room. After 4 weeks all rats were sacrificed. The mean pulmonary arterial pressure（m PAP） was measured by right-sided heart catheterization. The right heart hypertrophy index（RVHI） was calculated by the formula RV/（LV ＋ S） to evaluate the degree of right ventricular hypertrophy. Lung tissue microstructure morphology was observed on hematoxylin-eosin（HE） staining sections and Verhoeff-Van Gieson elastic（EVG） staining sections. The expression of HIF-1α, VEGF, TF in plasma was analyzed by ELISA. Results The m PAP, RVHI of rats in experiment group were significantly higher than those of control group（P〈0.05）. The pathological staining suggests obvious pulmonary arterial remodeling and situ thrombus in experimental group. The expression level of plasma HIF-1α, VEGF and TF in experimental group were significantly higher than those in control group（P〈0.05）. Conclusions The elevation of TF may partly responsible for the situ pulmonary thrombosis and hypercoagulable state in hypobaric hypoxia-induced pulmonary hypertension. The extrinsic route of blood coagulation may be related to pulmonary hypertension hypercoagulability.

关 键 词：低压低氧性肺动脉高压 大鼠模型 高凝状态 组织因子 

分 类 号：R544.1[医药卫生—心血管疾病]