Abstract: Abstract Objective To test the role of thrombospondin-1(TSP-1) and epidermal growth factor receptor (EGFR) in the development of hypoxic pulmonary hypertension. Methods Twenty male Wistar rats were divided into two groups and exposed to air and isobaric hypoxia for 3 weeks, respectively. The pulmonary artery pressure was measured by right cardiac catheterization. The expression of TSP-1 and EGFR in the lungs of rats were measured by immunohistochemical staining and in situ hybridization. The histological sections of the lungs were examined using a computerized image analyzer. Results The pulmonary artery pressure in the exposed rats increased. The chronic hypoxia also elicited the thicking of the wall and the narrowing of the lumen of pulmonary arterioles. It led to the increases of the pulmonary artery pressure 、the index of righr ventricular hypertrophy ﹝RV/(LV+S)﹞、 the ratio of vascular wall thickness/vascular external diameter(WA%) and the ratio of vascular wall area/total vascular area(WT%) compared to the controls (PAP2.86±0.39kP vs 1.35±0.28kP;﹝RV/(LV+S): 43.53±3.38 vs 23.68±3.48; WT%:35.24±11.2 vs 23.63±9.74; WA%:55.09±12.38 vs 41.62±12.83 respectively, p<0.05). The positive staining of TSP-1 protein and TSP-1mRNA in the wall of pulmonary arteriole of the exposed rats were significantly stronger than those of controls （P<0.01）, so as that of EGFR. Conclusions The TSP-1 and EGFR may play an important role in the pathogenesis process of hypoxic pulmonary vascular remodeling and pulmonary hypertension.

Key words: Hypoxia, Pulmonary hypertension, Pulmonary vascular remolding thrombospondin-1（TSP-1）, epidermal growth factor receptor（EGFR）