【摘 要】
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Objectives To observe the potential mechanism on pulmonary hypertension related right ventricle Remodeling in monocrotaline (MCT)-induced rats.Methods 12 male Sprague-Dawley rats were randomly divided
【机 构】
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Beijing Institute of Heart Lung and Blood Vessel Diseases-Captal Medical University affiliated Beiji
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Objectives To observe the potential mechanism on pulmonary hypertension related right ventricle Remodeling in monocrotaline (MCT)-induced rats.Methods 12 male Sprague-Dawley rats were randomly divided into 2 groups: control group and pulmonary arterialhypertension(PAH) group (induced by injection of MCT 60mg/kg).After 6 weeks, all survival rats were detected by echocardiography to observe the RV anterior wall diameter (RVAWd) and RV eject fraction (RVEF).All survival rats were measured by right catheterization to observe mean pulmonary artery pressure (mPAP).Right ventricle hypertrophy index (RVHI) were weighted.Collagen volume fraction (CVF) were detected.Expressions of AT1R, TGF-β1 and ERK1/2 protein of right ventricles tissue were determined by western blot.Results Compared with the control group, RVAWd, mPAP and RVWI significantly increased in PAH group ,RVHI[(25.01 ± 1.20)vs.(40.57±4.17)%], mPAP[(16.56± 1.98)vs.(29.46± 2.47)mmHg], RVAWd [(0.65± 0.09)vs.(1.17 ±0.08)mm], RVEF[(54.15±4.60)vs.(62.63±9.54)%], P<0.01 separately.CVF in PAH group was significant higher than that in control group (P<0.01).Compared with control group, AT1R, TGF-β 1 and ERK1/2 protein expression markedly increased (P<0.05) in PAH group.Conclusion In MCT-induced pulmonary hypertension related right ventricular remodeling rats, AT1R, TGF-β 1 and ERK1/2 protein expression of right ventricles were up-regulated.
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