Structural and functional changes of right ventricle in male rats with monocrotaline-induced pulmonary arterial hypertension
Objective To observe the structural and functional changes of right ventricle in male rats with pul-monary arterial hypertension(PAH)induced by monocrotaline(MCT),and to further clarify the mechanism of PAH.Methods SD rats were randomly divided into control group and model group with twelve rats in each group.The rats in the model group received a single subcutaneous injection of MCT at a dose of 40 mg·kg-1.Echocardiogra-phy was performed at 0,2,3 and 4 weeks after MCT injection to evaluate right ventricule function and right ventri-cle-pulmonary artery(RV-PA)coupling.At 4 weeks of MCT injection,mean pulmonary artery pressure(mPAP)was measured by right heart catheterization.Organs were removed and weighed to calculate organ coefficient and right ventricular hypertrophy index(RVHI).HE staining was used to observe the pathomorphological changes of pulmonary arterioles.The percentage of lumen area to the total vessel area(WA%)and the percentage of wall thickness to the outer radius of the vessel(WT%)were calculated.HE and Masson staining were adopted to ob-serve the degree of hypertrophy and fibrosis of RV cardiomyocytes.Results Compared with 0 week,RVFW and mPAP in the model group were increased(P<0.05).The levels of TAPSE,PA-AT,RVOT-VTI and PAT/PET,TAPSE/mPAP were decreased(P<0.05).RVID and TAPSE/PAT increased at 3 weeks(P<0.05).Compared with the control group,mPAP and RVHI were increased in the model group(P<0.05).In the model group,the wall of pulmonary arterioles was thickened,the media smooth muscle cells were proliferated and the lumen was nar-rowed.Besides,WA%and WT%were increased(P<0.05).Cardiomyocyte hypertrophy and myocardial fibrosis were observed in RV(P<0.05).The heart and lung of the model group were enlarged(P<0.05).Conclusion Pul-monary arterial hypertension induced by MCT is caused by the changes in right ventricle structure and function in rats with PAH.
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