Abstract:

 objective   To observe the inhibitive effect of enalapril on high-flow pulmonary hypertension in rats and to explore the mechanism of the Smad signaling pathway and connective tissue growth factor(CTGF) in pulmonary hypertension. Methods   Forty-five female Wistar rats were randomly divided into the sham operated group, the high-flow pulmonary hypertension group, and the enalapril group(each n=15).The rat model of pulmonary hypertension was established by  shunt operation between the abdominal aorta and inferior vena cava . The RVSP and RVHI were measured and WT% and WA% were calculated after HE staining of the left lung. Morphological changes of small pulmonary arteries were studied by microscopy. Expression of Smad7 and CTGF in the pulmonary arteries were determined by immunohistochemistry and Western blot, while expressions of CTGF and Smad7 mRNA were measured by reversetranscription polyme rase chain reaction(RT-PCR). Results   Compared with the sham-operated group, WT%、 WA%, RVSP, and RVHI, together with expressions of CTGF and CTGFmRNA, significantly increased in the high-flow pulmonary hypertension group. However, all these parameters  significantly deceased in the enalapril group when compared with the high-flow pulmonary hypertension group. Expressions of Smad7 and Smad7 mRNA in the high-flow pulmonary hypertension group were higher than those of the sham-operated group. Compared with the high-flow pulmonary hypertension group,  expressions of Smad7 and Smad7 mRNA in the enalapril group were increased. Conclusion   Enalpril may partly prevent the development of pulmonary hypertension by affecting CTGF and Smad7 in pulmonary hypertension rats.

Key words: Pulmonary hypertension； Connective tissue growth factor; Smad; Enalapril; Rat, Wistar