兔空气栓塞肺高压模型的建立和血管重构的研究

Establishment of Pulmonary Hypertension Model Induced by Continuous Pulmonary Air Embolization and Investigation of Vascular Remodeling in Rabbits

目的探讨空气栓塞建立家兔慢性栓塞肺动脉高压的可行性,并研究肺血管重构。方法将家兔随机分为4组:对照组(control,C)、空气栓塞1组(air embolization 1,AE1)、空气栓塞2组(AE2)、空气栓塞3组(AE3),经过多次预实验的总结,后3组每日分别经家兔耳缘静脉注入洁净空气0.6ml[0.05ml/(min·kg)]、0.8ml和1.0ml,连续28天后测定4组家兔肺动脉收缩压(PASP)、舒张压(PADP)、平均肺动脉压(m PAP)和右心室肥厚指数(RVHI),内皮素-1测定;光镜下结合图像软件观测肺小动脉的病理变化,中膜厚度比值(WT),新生内膜和血管阻塞计分(VOS)。结果与C组肺动脉压力和RVHI、内皮素-1比较,AE1组差异无统计学意义(P均>0.05),AE2组PADP和RVHI比较差异无统计学意义(P均>0.05),PASP、m PAP和内皮素-1比较差异有统计学意义(P>0.05),AE3组均显著增高(P均<0.05)。肺小动脉病理:与C组比较,AE1组肺小动脉未见变化,AE2组肺小动脉管壁增厚、管腔狭窄,WT,新生内膜形成和VOS均出现轻度改变(P均<0.05),AE3组肺小动脉管壁明显增厚、管腔狭窄,WT,新生内膜形成和VOS均升高(P均<0.05)。结论家兔持续空气栓塞28天后成功建立肺动脉高压模型,出现肺血管重构。该模型较为理想、经济。

Objective To establish the model of the chronic pulmonary hypertension induced by continuous pulmonary air embolization in rabbits and to investigate the pulmonary vascular remodeling. Methods A total of 44 rabbits were randomly divided into control group,air embolization 1 group,air embolization 2 group and air embolization 3 group.In the latter three air embolic groups filtered air were continuously infused into rabbits through ear vein about 0.6ml[0.05ml/（min·kg）],0.8ml[0.05ml/（min·kg）] and 1.0ml[0.05ml/（min·kg）],which were recevied continuous air embolization for 28 days,then pulmonary artery pressures （PASP,PADP, mPAP）,RVHI and Endothelin-1 were measured.morphological parameters relevant to pulmonary vascular remodeling were performed in three groups,including pathological changes of small pulmonary arteries,medial thickness,neointima formation and vascular occlusion scores（VOS）. Rseults Comparing with control group,the PAP（PASP,PADP, mPAP）、RVHI and Endothelin-1 in air embolization 1 group had no difference（P〉0.05）, the PADP and RVHI in air embolization 2 group had no difference（P〉0.05）, and others had differences（P〈0.05）.These in air embolization 3 group were all significant differences,respectively（P〈0.05）.Comparing with control group,the pathological changes in air embolization 1 group had no difference（P〉0.05）.However,the thickness of the small pulmonary arteries, medial thickness, neointima formation and vascular occlusion scores（VOS） increased in air embolization 2 and air embolization 3 groups,respectively（P〈0.05）.Moreover,these in air embolization 3 group all had all significant differences. Conclusion We could conclude that our 28-day model of continuous air embolism produced chronic air embolization pulmonary hypertension,significant pulmonary vascular remodeling.This model is ideal and economic.