Characteristics Of Pulmonary Hypertension Model In Rats

Objective: To establish the model of pulmonary hypertension and compare the characteristics of pulmonary hypertension model established by different typers of different types of pulmonary hypertension and the treatment of pulmonary hypertension,Methods: Twenty-four male SD rats were randomly divided into four groups: normoxic group(n = 6),hypoxia group(n = 6),MCT group(n = 6)and SU5416 group(n = 6).The rats were anesthetized after 4 weeks,and the rats were killed after(mPAP)was measured by right cardiac catheterization.The heart was cut to measure the right cardiac hypertrophy index,HE staining was used to observe the morphological changes of the lung tissue,and the pulmonary vascular thickening index(WT%,WA%.)was observed.Results:1.In normoxic group,mPAP was normal(12.3±2.1 mmHg);RVHI(22.55%);Under HE staining electron microscope,The alveolar wall and alveolar septum were normal,and the pulmonary arterioles were not thickened or narrowed;WT(21.2±2.1)%,WA(36.6±2.1%).2.In hypoxia group,mPAP increased(31.2±2.1 mmHg);RVHI(66.58%).Under HE staining electron microscope,the alveolar wall became thinner,the alveolar septum narrowed or ruptured,and the pulmonary arterioles were slightly thickened,accompanied by a small amount of inflammatory cell infiltration,which was similar to the pathological manifestation of emphysema.WT(35.21±11.1)%,WA(56.5±5.1)%.3.In MCT group,mPAP increased significantly(42±3.2 mmHg);RVHI(60.8%).Under HE staining electron microscope,extensive widening of alveolar septum,thickening of muscle layer of pulmonary arterioles with intimal hyperplasia were observed,and more inflammatory cell infiltration was observed,which was similar to II grade of idiopathic pulmonary hypertension.WT was(69.1±0.1)%,WA(80.2±2.3%).4.In hypoxia SU5416 group,mPAP increased significantly(42.9±5.8 mmHg);RVHI)(66.58%).Under HE staining electron microscope,extensive widening of alveolar septum,neointimal formation between lateral endothelial cells and internal elastic plate,extensive fibrosis of intima and media of pulmonary arterioles,slave lesions and stenosis of lumen were observed.In some severe cases,the lumen has been completely occlusive,accompanied by more inflammatory cell infiltration,which is similar to the pathogenesis of severe idiopathic pulmonary hypertension.WT(72.33±0.2)%,WA(85.3 ±1.8)%.5.MPAP,RVHI,WT%,WA% in hypoxia group,MCT group and hypoxia SU5416 group was higher than that in normoxic group(P < 0.05).MCT).MPAP,RVHI,WT%,in hypoxia SU5416 group was significantly higher than that in normoxic group(P < 0.05).WA% was higher than that in hypoxia group(P < 0.05).MPAP in MCT group was higher than that in hypoxia SU5416 group(P < 0.05).MCT group.There was no significant difference in RVHI,WT%,WA% in hypoxia SU5416 group(P > 0.05).Conclusions:1.Hypoxia and MCT,hypoxia SU5416 can increase pulmonary artery pressure,which leads to right ventricular hypertrophy and hypoxia induced pulmonary hypertension.2.The pathogenesis of pulmonary hypertension is similar to that of human chronic obstructive pulmonary disease.3.The pathogenesis of pulmonary hypertension induced by MCT is similar to that of human idiopathic pulmonary hypertension.4.The pathogenesis of pulmonary hypertension induced by hypoxia SU5416 is most similar to that of severe idiopathic pulmonary hypertension in humans.5.Hypoxia SU5416 was more significant than MCT induced pulmonary hypertension model.