Inhaling one hundred percent oxygen eliminates the systemic arterial hypoxemic response of broilers to intravenous microparticle injections

The pathogenesis of pulmonary hypertension syndrome (PHS, ascites) includes the development of systemic arterial hypoxemia (reduction in the saturation of hemoglobin with O₂, HbO₂), which can be mimicked in clinically healthy broilers by i.v. injections of microparticles (MP). In experiment 1, arterial blood samples were collected from clinically healthy broilers before and after i.v. MP injections, and during a subsequent 100% O₂ inhalation period. The arterial samples were analyzed for HbO ₂, partial pressure of O₂ and CO₂, and pH using a blood gas analyzer. In experiment 2, broilers that initially averaged ≥75% HbO₂ were assigned to a "high O₂" group, whereas those that initially averaged <75% HbO₂ were assigned to a "low O₂" group. The HbO₂ and heart rate (HR) were measured using a pulse oximeter before, during, and after broilers in both groups inhaled 100% O₂. In experiment 3, HbO₂ and HR were measured using a pulse oximeter before, during, and after broilers inhaled 100% O₂, after i.v. MP injections, and during a second period of 100% O₂ inhalation. The HbO₂ rapidly decreased after i.v. MP injections, and subsequently providing 100% O₂ to breathe increased the HbO₂ above preinjection control levels in experiments 1 and 3. In experiment 2, inhaling 100% oxygen eliminated the initial spontaneous differences in HbO₂ between the high O₂ and low O ₂ groups, whereas the return to breathing ambient air restored the initial group differences in HbO₂. These experiments indicate that MP-induced and spontaneous hypoxemia can be attributed to a diffusion limitation rather than to arterial-venous shunts, because the hypoxemia resulting from arterial-venous shunts cannot be wholly eliminated by providing 100% O ₂ to inhale.