Mechanism Of Smad Signaling Pathway And Connective Tissue Growth Factor In The Inhibition Of Pulmonary Hypertension In Rats By Enalapril

BACKGROUND Patients with congenital heart disease are usually associated with a lot of neopathy,and pulmonary arterial hypertension is the most common complication which affacts the prognosis of patients. The current treatments mainly includes pharmacotherapy,Surgery. The patients that are not suitable for surgery or their postoperative function are not improved can use drug therapies.The drugs,such as nitric oxide, prostaglandin inhibitors of phosphodiesterase and endothelin antagonists are widely used to treat pulmonary arterial hypertension. Because there are lots of elements involved in the pathogenesis of pulmonary hypertension,its pathogenesis is still unknown. There is no satisfactory therapy for it. Regular monitoring, it's important to Clear the pathogenesis of pulmonary hypertension and seek more effective treatments for pulmonary arterial hypertension treatment.OBJECTIVE To observe the inhibitive effect of enalapril on high-flow pulmonary hypertension in rats and to explore the mechanism of Smad signaling pathway and connective tissue growth factor(CTGF) in the pulmonary hypertension by enalapril.METHODS Forty-five famale wistar rats were randomly divided into a shamoperated group,a high-flow pulmonary hypertension group,a enalapril treated group (n=15each). The rat model of pulmonary hypertension was established by underwent abdominal aorta and inferior vena cava shunt operation. Measuring the RVSP and RVHI in each group and calculating WT% and WA% after HE staining the left lung.The small pulmonary arterial morphologic changes in each groups were studied with microscopy for morphometric analysis.The expression of Smad7 and CTGF by pulmanory arteries were determined by immunohistochemistry and western blot.RESULTS Compared with shamoperated group,the pulmonary arterial morphologic changes in the high-flow pulmonary hypertension group showed that the WT%,WA% and RVSP,RVHI (P<0.01) togther with the expression of CTGF (P<0.05) increased significantly.However in enalapril treated group,they are deceased significantly than the high-flow pulmonary hypertension group (P<0.01).The expression of Smad7 (P<0.05) in high-flow pulmonary hypertension group was increased compared with shamoperated group.Compared with high-flow pulmomary hypertension group,the expression of Smad7 (P<0.05) in enalapril treated group was increased.CONCLUSIONS Enalapric may partly prevent the development of pulmanory hypertension by affecting CTGF and Smad7 of the pulmonary hypertension rats.