Flow-dependent pulmonary vasodilation during acute unilateral pulmonary artery occlusion in Jungle Fowl

Giant Jungle Fowl previously were shown to be highly resistant to the onset of pulmonary hypertension syndrome (PHS, ascites) under conditions that induce a substantial incidence of PHS in broiler chickens. In the present study, lightly anesthetized, clinically healthy 12- to 13-wk-old male Giant Jungle Fowl maintained a lower respiratory rate, a similar hematocrit, and superior arterial blood gas values when compared with 6-wk-old male broilers. Giant Jungle Fowl weighed less than broilers (1,860 +/- 19 vs 2,788 +/- 63 g, respectively) and had equivalent absolute values for pulmonary arterial pressure, cardiac output, and pulmonary vascular resistance. Acute unilateral pulmonary artery occlusion in Giant Jungle Fowl doubled the pulmonary vascular resistance and forced the right ventricle to propel a sustained 60% increase in blood flow through the vasculature of the unoccluded lung. A transient increase in pulmonary arterial pressure initially was required to overcome the vascular resistance of the unoccluded lung; however, flow-dependent vasodilation gradually reduced the pulmonary vascular resistance and permitted pulmonary arterial pressure to return toward control levels. Unilateral pulmonary artery occlusion also triggered an immediate reduction in the partial pressure of oxygen in arterial blood, and the gradual return of pulmonary arterial pressure toward control levels did not eliminate this ventilation-perfusion mismatch, which has been attributed to blood flowing too rapidly through the unoccluded lung to permit diffusive gas equilibration. The inherent capacity for flow-dependent pulmonary vasodilation may reduce the susceptibility of Giant Jungle Fowl to PHS by reducing the increment in pulmonary arterial pressure required to propel an elevated blood flow through the lungs.