So as to understand better the pathogenesis of enlargement or hypoplasia of pulmonary arteries in congenital heart disease, we studied the dimensions of the pulmonary arteries in 74 fetuses with congenital heart disease induced by administration of bis-diamine to pregnant rats. The congenital malformations induced included 12 with large ventricular septal defect, 17 with tetralogy of Fallot, 15 with tetralogy together with severe valvar pulmonary stenosis and absence of the arterial duct, 17 with tetralogy with absent pulmonary valve syndrome and absence of the arterial duct, and 13 with common arterial trunk with a confluent segment supplying the pulmonary arteries. For comparison, 16 fetuses of the same gestational age with normal hearts were studied. After rapid whole-body freezing on the 21st day of gestation, the fetuses were studied by means of serial cross-sectional photographs of the thorax. The diameter of the right pulmonary artery of the fetus was of comparable dimensions in the normal hearts (480±10 µm) (mean±SEM), those with ventricular septal defects (470±10 µm), common arterial trunk (520±20 µm), and tetralogy of Fallot (500±10 µm). These findings suggest that the commonly observed enlargement of the right pulmonary artery in patients with ventricular septal defect and common arterial trunk, and hypoplasia of the right pulmonary artery in tetralogy of Fallot, occur postnatally in response to abnormal postnatal pulmonary blood flow.