A small experimental animal model of postobstructive pulmonary hypertension (PH) providing insights in the physiopathology of this disease was developed.Male Lewis rats were anesthetized and aleatory manipulated via a left thoracotomy with (group I, n = 10) or without (group II, n = 10) ligation of the left pulmonary artery. Animals were followed for 2 weeks and then sacrificed. Hemodynamic parameters and blood gases were recorded at baseline and 2 weeks after surgical procedure.Group I animals developed a significant (P < 0.01) PH (mean pulmonary artery pressure, 32 ± 6 versus 16 ± 2 mm Hg; pulmonary vascular resistance, 46 ± 3 versus 21 ± 2 mm Hg/mL/min; reduction of cardiac output, 75 ± 3 versus 105 ± 4 mL/min), compared to group II animals, and had a significant (P < 0.01) worse gas exchange (partial arterial pressure of O 2 : 91 ± 3 versus 439 ± 24 mm Hg; partial arterial pressure of CO 2 : 54 ± 3 versus 42 ± 2 mm Hg, on a fraction of inspired oxygen of 1.0), right ventricle hypertrophy (ventricle to left ventricle/septum ratio, 0.56 ± 0.04 versus 0.45 ± 0.04, P < 0.02) and less tolerance test (immobility time, 123 ± 11 versus 61 ± 8 s, P < 0.01) than group II animals. Histologically, ligated lungs showed postobstructive pulmonary vasculopathic abnormalities and bronchial-pulmonary artery hypertrophy, and the contralateral lung had initial signs of small vessel arteriopathy.The experimental model generated here successfully reproduced a PH morphologically and functionally similar to clinical postembolic PH and might be used for evaluating the physiopathology of postobstructive PH.