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 conditio ns 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 s imilar hematocrit, and superior arterial blood gas values when compare d with 6-wk-old male broilers. Giant Jungle Fowl weighed less than bro ilers (1,860 +/- 15, vs 2,788 +/- 63 g, respectively) and had equivale nt absolute values for pulmonary arterial pressure, cardiac output, an d pulmonary vascular resistance. Acute unilateral pulmonary artery occ lusion in Giant Jungle Fowl doubled the pulmonary vascular resistance and forced the right ventricle to propel a sustained 60% increase in b lood flow through the vasculature of the unoccluded lung. A transient increase in pulmonary arterial pressure initially was required to over come the vascular resistance of the unoccluded lung; however, flow-dep endent vasodilation gradually reduced the pulmonary vascular resistanc e and permitted pulmonary arterial pressure to return toward control l evels. Unilateral pulmonary artery occlusion also triggered an immedia te reduction in the partial pressure of oxygen in arterial blood, and the gradual return of pulmonary arterial pressure toward control level s did not eliminate this ventilation-perfusion mismatch, which has bee n 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 Gian t Jungle Fowl to PI-IS by reducing the increment in pulmonary arterial pressure required to propel an elevated blood flow through the lungs.