During fetal development, pulmonary vascular resistance (PVR) is high, and, as a result, blood flow through the fetal lungs is low. Although PVR markedly decreases at the time of birth, the factors that regulate pulmonary blood flow (PBF) and PVR before and immediately after birth are not clear. Our aim was to examine the relationship between episodes of fetal breathing movements (FBM) and pulmonary hemodynamics during late gestation to further understand the relationship among lung luminal volume, phasic changes in intrapulmonary pressure, and PVR before birth. In chronically catheterized fetal sheep (120 -128 d gestation; n ϭ 5; term~147 d), PBF and PVR were measured during periods of FBM and apnea. Episodes of FBM were divided into periods of accentuated (amplitude of Ͼ3.5 mm Hg change in tracheal pressure) and nonaccentuated periods of FBM. During accentuated episodes of FBM, mean PBF was increased to 159.5 Ϯ 23.4% (p Ͻ 0.0025) of the preceding apneic period and was associated with a 19.1 Ϯ 5.2% reduction in PVR. In addition, during accentuated episodes of FBM, the retrograde flow of blood through the left pulmonary artery was reduced to 90.1 Ϯ 1.0% of the preceding apneic period, which most likely contributed to the increase in mean PBF at this time. Although a change in PBF and PVR could not be detected during nonaccentuated FBM, compared with the preceding apneic period, PBF was linearly and positively correlated with the amplitude (change in pressure) of FBM. We conclude that PVR is decreased and PBF is increased during accentuated episodes of FBM, possibly as a result of phasic reductions in intrapulmonary pressures. At birth, blood flow through the lungs markedly increases as a result of a large reduction in pulmonary vascular resistance (PVR). Although this process plays a vital role in the transition from intra-to extrauterine life, the precise mechanisms involved are still not clear. In particular, it is not clear why PVR is high in the fetus, relative to the newborn. During fetal life, the majority (88%) of right ventricular output bypasses the lungs and is shunted into the systemic circulation via the ductus arteriosus (1). In the late-gestation fetus, the relatively high PVR has been attributed to the low PO 2 of blood perfusing the lungs (2,3), to the balance between vasoconstrictor and vasodilator activity (4 -7), and to the high level of resting lung expansion in the fetus (8).Previous studies have investigated the relationship between lung luminal volume and PVR in the fetus and have shown that PVR is directly proportional to the changes in lung volume, causing pulmonary blood flow (PBF) to cease at total lung capacity (9). Conversely, a reduction in lung liquid volume, to a volume that is equivalent to the end-expiratory lung volume in the air-filled lung after birth, caused a 3-to 4-fold increase in PBF and a substantial decrease in PVR (8). Together, these studies indicate that the degree of lung expansion and the associated change in intraluminal pressure may be important physiologic dete...