Effect of Monocrotaline on Over-expression of α-Smooth Muscle Actin and Low-expression of VIII Factor Antigen on Pulmonary Arteries in Rats

Objective To study the effect and mechanisms of monocrotaline(MCT)on the pulmonary arterial pressure.Methods Eighteen Sprague-Dawley male rats were randomly divided into normal control group(n=7)and model group(n=11).Animals in the model group were given with a single dose of MCT(50 mg·kg-1)subcutaneously.Hemodynamic parameters such as pulmonary arterial systolic pressure(PASP),pulmonary artery diastolic pressure(PADP),mean pulmonary arterial pressure(MPAP)and right ventricular systolic pressure(RVSP)were measured by right catheterization with Powerlab on the 22nd day.The heart was separated into the right ventricle(RV)and left one with septum(LV+SEP)and weighed separately.RVHI was calculated as the weight ratio of RV/(LV+SEP).The weight ratio of lung to body weight was calculated.Immunohistochemical analysis was performed on paraffin-embedded left lung tissue to detect the expression of α-smooth muscle actin(α-SMA)and Ⅷ factor on pulmonary endangium.Results The PASP,PADP,MPAP and RVSP were elevated significantly(P0.01)in the 50 mg·kg-1MCT-treated rats as compared with the normal control animals.The similar changes were observed for the values of LI and RVHI(P0.01).Immunohistochemical analysis showed MCT effectively increased the expression of α-SMA antigen in pulmonary arteries(PAs)and lead to PAs remodeling.In addition,MCT also could effectively decrease the expression of Ⅷ factor antigen in the endomembrane of PAs and lessen the number of pulmonary capillary.Conclusion MCT(50 mg·kg-1)can satisfactorily make the model of pulmonary artery hypertension and the mechanism of which may be related to the PA remodeling and the loss of pulmonary capillary.