Objective To investigate the mechanism and significance of low density nitric oxide (NO) in-halation combined with urokinase (UK) in treatment of pulmonary thromboembolism in swine. Method PIE model was estabhshed in 12 healthy infant swines, which were subsequently assigned to UK group or UK+NO ter establishment of the PIE model;in the UK+NO group, swines received continuous NO inhalation of 10 ppm NO for two hours in addition to administration of UK no done in the UK+NO group. Volume of physiological dead space (VDphy), volume of alveolar dead space (VDalv), intrapoulmonary shunt (Qs/Qt), mean ptdmonary arteri-al pressure (PAP), systolic blood pressure (SBP), heart rote (HR), cardiac output (CO), arterial blood pH val-ue, arterial partial pressure of carbon dioxide (PaCO2) and arterial partial pressure of oxygen (PaO2) were mea-sured at 30 min before and 0 min, 30 min, 60 rain, 120 min and 180min after establishment of pulmonary em-bolism.All date were analyzed by ANOVA (SNK-q test),and P<0.05 was considered as significantly differet. Results After PE, VDphy, VDalv, Qs/Qt and PAP of both groups increased markedly compared with the pre-PE values (P<0.01), but the post-PE PAP showed a tendency of decline as time passed. Post-PE PaO2 of both groups decreased significantly (P<0.05 and P<0.01). There were no significant differences in HR, SBP, CO, pH or PaCO2 between pre-PE and post-PE (P>0.05). Both pre- and Post-PE PAP of UK+NO group were markedly less than those of the UK group (P<0.05 and P<0.01). No significant difference was found in other measurements between the two groups. Conclusions UK combined with low density NO inhalation may lower pul-monary arterial pressure promptly to alleviate PIE without distur bance in hemodynamics or gas exchange status and without pulmonary raterial pressure rebound.