The lungs of domestic chickens were perfused with blood or dextran/saline and the pulmonary artery pressure (Pa) and venous pressure (Pv) were varied in relation to air capillary pressure (PA). In zone 3 conditions, pulmonary vascular resistance (PVR) was virtually unchanged with increases in either Pa or Pv. This is very different from mammals where the same interventions greatly reduce PVR. In zone 2 conditions blood flow was essentially independent of Pv as in mammalian lungs but all the capillaries appeared to be open, apparently incompatible with a Starling resistor mechanism. In zone 1 the capillaries were open even when PA exceeded Pa by over 30 cmH 2 O which is very different behavior from that of the mammalian lung. We conclude that the air capillaries that surround the blood capillaries provide rigid support in both compression and expansion of the vessels. The work suggests a pathogenesis for Pulmonary Hypertension Syndrome in chickens which costs the broiler industry $1 billion per year.