A porcine model was produced to study the pathophysiology of congenital heart defect (CHD) with decreased pulmonary blood flow. Twenty piglets (1-2 months) were randomly divided as mild to moderate stenosis/T(1) group (n = 7) in which artificial atrial septal defect (ASD) with pulmonary artery banding generated a systolic pressure gradient of 20-30 mmHg; severe stenosis/T group (n = 7) group with a systolic pressure gradient of ≥30-50 mmHg; and controls/C group (n = 6) underwent sham surgery. At 1 month postoperatively, 64-slice computed tomography (CT) was performed. At 2 months, left-chest surgery was performed to measure ASD diameter, arterial blood gas, hemoglobin, and Trans-PABP. Our data show successful establishment of porcine CHD model. ASDs in T(1)/T(2) groups were 8.0 ± 0.5/8.9 ± 1.4 mm, respectively. Trans-PABP showed that the pressure increase in T(2) was higher (P < 0.01) than in T(1) group. Arterial blood PaO(2) and SaO(2) of T(1/)T(2) groups were significantly lower than controls. AoD was significantly lower in T(1) than in C group. Balloon dilation was significantly lower than AoD in T(1)/T(2) groups. Besides, one animal in T(1), two animals in T(2) ,and one animal in C group died. We conclude that ASD with pulmonary artery banding is a successful intervention to establish such a model, and our findings may influence the treatment of patients with similar heart disease.