In this paper, we studledthe mechanical properties of canine pulmonary arterles under acute pulmonary hypertenslon. The condltion was induced by infusion of the thromboxane A2 analogue U46619 using right heart catheterization techniques. The theoretical study was based a Windkessel Model. The results demonstrated a mlnimal difference of cardiac output (CO) (1.85- 0.21 vs 1.21 - 0.25 lml, P0.05) before and after the induced condition of acute pulmonary hypertension.However the results showed a significantly!ffle in pulmonary vessel resistance (PVR) under the induced condition as compared with the normal situation (31.4- 9.4 vs 148.7 12.3kPa s/L,P<0.01). As of the pulmonary arterlal compliance, Cm decreased noticeably (12.43 - 2.62 vs 10.30 - 3.12ml/kPa, P<0.05), while Co had only negligible variation. These results suggested that the change of PVR caused by small pulmonary artery contraction was a main factor influencing the acute pulmonary hypertension, therefore, the vasodi1ator which dilate small arterles was the optimal cholce in treating acute pulmonary hypertension.