Objective To establish a canine model with pulmonary thromboembolism(PTE) of selective lobar pulmonary artery embolization mimicking chronic thromboembolism, to assess the effects of an inhaled nitric oxide (NO) 20 ppm on vital signs, blood gas, hemodynamic parameters and neutrophils in the alveolar of the canine model. Methods Twenty canines were divided into four groups: group 1: sham group (n=5); group 2; ischemic lung group (PTE group without embolectomy, n=5); group 3; reperfusion lung group (PTE group with embolectomy, n=5); group 4: reperfusion lung group with inhaled NO (PTE group inhaled 20 ppm NO after embolectomy, n=5). And central venous pressure (CVP), mean pulmonary arterial pressure (MPAP), pulmonary arterial wedge pressure (PAWP) and carbon monoxide (CO) were recorded, pulmonary vascular resistance (PVR) was also calculated. Vital signs, blood gases were measured before embolectomy and at 2, 4, 6 hours after the operation. Albumin in bronchoalveolar lavage fluid (BALF) was measured by chromatometry of Coomassie brilliant blue. Lung wet to dry weight ratio(W/D) was also measured. Lung tissue pathology and alveolar PMN in the left lower lobar were observed by optical microscopy. Results MPAP increased significantly at 2 hours after reperfusion [(3. 20±0.53)kPa vs. (2. 27±0. 67)kPa,F=63,P=0.02]; At 6 hours after reperfusion as compared with baseline,HR increased significantly [(175±8) beats/min vs. (155±5) beats/min, F=38.72, P=0.01],PaO_2/FiO_2 also decreased significantly (41.70±8.04 vs. 54.71±3.78,F=48.36,P=0.03). MPAP decreased significantly in group 4 as compared with group 3 at 2 hours after reperfusion [(2.53±0.4)kPa vs. (3. 20±0. 53)kPa,F=55,P=0.04]. At 4 hours after reperfusion,PaO_2/FiO_2 raised in group 4,but there was no significant difference as compared with group 3 (49.17±7.37 vs. 39.71±7.31, F=2.36, P=0. 11). The quantities of alveolar PMN infiltration in group 4 decreased significantly as compared with group 3 (19±6/10 HPF vs. 31±11/10 HPF, F=98, P=0.01).Conclusions Lung ischemia-reperfusion injury can be induced by embolectomy from lower pulmonary artery in the PTE model embolized for one week. An inhaled NO 20 ppm can decrease the elevated pulmonary artery pressure induced by ischemia-reperfusion injury and may alleviate the injury by reducing the PMN immigration into the alveoli.