Abstract: Objective To investigate the influences of transfection of adenovirus-mediated p53 knockdown gene(Adeno-p53) on the pressure of the pulmonary artery and apoptosis of smooth muscle cells in pulmonary arteries of rats under hypoxia. 
Methods Sixty SD rats were randomly divided into 6 groups(n=10): normoxic control group, normoxic experiment Adeno-null group, normoxic experiment Adeno-p53 group, hypoxic control group, hypoxia experiment Adeno-null group, hypoxic experiment Adeno-p53 group. Pulmonic hypertension in the hypoxia groups was induced in a hypoxic chamber by exposing the rats to an isobaric atmosphere containing 10% O2. During the third week, 3×108 MOI titers Adeno-p53 and Adeno-null were dropped into the trachea below epiglottis for the experimental groups respectively, and the culture was continued for 2 weeks. The mean carotid artery pressure and the mean pulmonary arterial pressure were measured by right heart catheterization. The right ventricle, ventricular septum, and left ventricle were weighed and the right ventricular hypertrophy index was calculated. The apoptotic index of pulmonary artery smooth muscle cells was detected by TUNEL staining in the left lung tissues. Influences of p53-knockdown gene on the pressure of the pulmonary and smooth muscle cell apoptosis were evaluated. 
Results Compared with the rats cultured under normal pressure, the rats that continuously cultured in 10.0% O2 for 4 weeks had a significantly higher mean pulmonary artery pressure and right ventricular hypertrophy(P＜0.01 or P＜0.05). Under hypoxia culture conditions, compared with the hypoxia experiment Adeno-null group, the hypoxia experiment Adeno-p53 group had lower pulmonary artery pressure and right ventricular hypertrophy index(P＜0.05). The apoptosis index of pulmonary artery smooth muscle cells in the hypoxia experiment Adeno-p53 group was significantly higher than that of the hypoxia experiment Adeno-null group, The apoptosis index of pulmonary artery smooth muscle cells in the Adeno-p53 group was higher than that of the Adeno-null group(P＜0.05). 
Conclusion The p53 knockdown gene can alleviate the development of hypoxic pulmonary hypertension, which may be related to the apoptosis of vascular smooth muscle in the pulmonary artery induced by the p53 gene.

Key words: hypertension, pulmonary, p53 knockdown gene, adenoviruses