Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp ditions, again, remain uncertain.Experimental studies in animal models, including our own, have used exposure of pregnant mammals to chronic hypobaric or isobaric hypoxia during gestation and have studied the effects on fetal growth and on the cardiovascular system of the offspring in the newborn and adult periods. 21-23 Studies such as these have reported that chronic fetal hypoxia can program persistent pulmonary hypertension in the newborn and pulmonary hypertension in the adult offspring. 24 However, because maternal exposure to hypoxia can lead to a significant decrease in maternal food intake, 25 the extent to which any adverse effects on the pulmonary circulation of the offspring are due to under-nutrition and/or under-oxygenation, once again, remain unclear.The combination of HA exposure with the use of the chick embryo model permits investigation of the direct effects of HA hypoxia on growth and on cardiovascular development completely independent of alterations in placental function, independent of changes in the maternal physiology and independent of any effects of socioeconomic factors. Previously, we ulmonary hypertension continues to be an important clinical problem. 1-8 Studies of populations at high altitude (HA) have unequivocally reported intrauterine growth restriction (IUGR) and a higher prevalence of pulmonary hypertension, 9-17 suggesting that a component of these conditions is associated with exposure to chronic hypoxia. However, because most highland populations are also impoverished, the relative contributions of chronic hypoxia or of chronic malnutrition during the fetal and postnatal periods in stunting growth and promoting pulmonary vascular disease during life at altitude remain uncertain.Similarly, clinical studies at sea level (SL) have reported an association between the IUGR infant and the early development of right ventricular dysfunction and pulmonary hypertension. 18-20 However, because IUGR in human high-risk pregnancy normally occurs as a result of increased placental vascular impedance with consequent falls in oxygen and nutrient delivery to the baby, the relative contributions of chronic hypoxia or of chronic malnutrition during the fetal period in slowing growth and promoting pulmonary vascular anomalies under these con- Background: By combining the chick embryo model with incubation at high altitude (HA), the effects of chronic hypoxia on fetal growth, fetal cardiac and aortic wall remodeling and systemic arterial blood pressure at adulthood were reported. Using non-invasive functional echocardiography, here we investigated the in vivo effects of HA hypoxia on the pulmonary circulation at adulthood in male and female chickens.