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

The pathogenesis of pulmonary hypertension syndrome (PHS, ascites) includes the development of systemic arterial hypoxemia (reduction in the saturation of hemoglobin with O(2), HbO(2)), 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% O(2) inhalation period. The arterial samples were analyzed for HbO(2), partial pressure of O(2) and CO(2), and pH using a blood gas analyzer. In experiment 2, broilers that initially averaged > or =75% HbO(2) were assigned to a "high O(2)" group, whereas those that initially averaged < 75% HbO(2) were assigned to a "low O(2)" group. The HbO(2) and heart rate (HR) were measured using a pulse oximeter before, during, and after broilers in both groups inhaled 100% O(2). In experiment 3, HbO(2) and HR were measured using a pulse oximeter before, during, and after broilers inhaled 100% O(2), after i.v. MP injections, and during a second period of 100% O(2) inhalation. The HbO(2) rapidly decreased after i.v. MP injections, and subsequently providing 100% O(2) to breathe increased the HbO(2) above preinjection control levels in experiments 1 and 3. In experiment 2, inhaling 100% oxygen eliminated the initial spontaneous differences in HbO(2) between the high O(2) and low O(2) groups, whereas the return to breathing ambient air restored the initial group differences in HbO(2). 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.