Broilers from three consecutive hatches were exposed to cool temperatures to amplify the incidence of pulmonary hypertension syndrome (PHS, ascites). The largest apparently healthy individuals on Day 42 were evaluated using minimally invasive diagnostic indices [percentage saturation of hemoglobin with oxygen, hematocrit (HCT), heart rate, electrocardiogram (ECG) Lead II, body weight), then they were subjected to the ongoing pressures of fast growth and cool temperatures to determine which of these indices are predictive of the subsequent onset of PHS. Approximately 20% of the males and females evaluated on Day 42 subsequently developed PHS by Day 51. When data for all hatches were pooled and broilers that subsequently developed ascites were compared with those that did not (nonascitic), body weights, heart rates, and percentage saturation of hemoglobin with oxygen were lower on Day 42 for ascitic than for nonascitic males, and HCT was higher in ascitic males and females than in nonascitic males and females, respectively. Comparisons of the ECG Lead II wave amplitudes for all hatches pooled indicated that RS-wave amplitude was larger in ascitic than in nonascitic males, and that S-wave amplitude was more negative in ascitic males and females than in nonascitic males and females. Necropsies conducted on Day 51 revealed higher right:total ventricular weight ratios in ascitic than in nonascitic broilers, whereas normalizing the left ventricle plus septum weight for differences in body weight generated similar values for ascitic and nonascitic males and females, respectively. These results support a primary role for pulmonary hypertension but not cardiomyopathy in the pathogenesis of ascites triggered by cool temperatures. Values obtained for minimally invasive diagnostic indices on Day 42 also establish predictive thresholds that can be used to evaluate the PHS susceptibility of large and apparently healthy male and female broilers.

Cardio-pulmonary function was measured in male broilers reared on diets formulated to contain 1.5% arginine (NORMAL group) or 2.5% arginine (ARGININE group). A snare placed around the right pulmonary artery permitted acute shunting of the entire cardiac output (CO) through the left pulmonary artery, resulting in sustained increases in blood flow (BF) through the left lung in both groups. The unilateral increase in BF was accompanied by sustained increases in pulmonary arterial pressure (PAP) and pulmonary vascular resistance (PVR) in the NORMAL group. However, following initial transient increases in PAP and PVR in the ARGININE group, subsequent pulmonary vasodilation gradually reduced PVR, and thus PAP, in spite of the ongoing elevation of BF through the left lung. The capacity of the pulmonary vasculature in the ARGININE group to accommodate an increased BF at a normal PAP accounts for the previously reported lower incidence of pulmonary hypertension syndrome (PHS, ascites) in cold-stressed broilers fed supplemental dietary arginine. Hypoxemia and respiratory acidosis ensued rapidly in both groups after tightening the pulmonary artery snare, in spite of a compensatory increase in the respiratory rate. The gradual return of PVR and PAP to presnare levels in the ARGININE group did not eliminate the concurrent ventilation-perfusion mismatch caused by the increased rate of BF through the left lung. Tightening the pulmonary artery snare caused mean systemic arterial pressure (MAP) to drop from control levels of approximately 98 mm Hg to sustained hypotensive levels of approximately 65 mm Hg in both groups. This systemic hypotension was caused by decreases in CO and total peripheral resistance (TPR). The reduction in CO were caused by reduction in stroke volume (SV) rather than heart rate (HR), suggesting that acutely tightening the pulmonary artery snare increased PVR sufficiently to impede left ventricular filling. Accordingly, the maximum increment in PAP attainable by the right ventricle during acute increases in PVR apparently was inadequate to propel the entire CO through the pulmonary vasculature, setting the stage for the congestive right-sided pooling of blood routinely associated with PHS in broilers.

Fast growth and cool temperatures are the primary triggers for pulmonary hypertension syndrome (PHS, ascites) during commercial broiler growout. We evaluated cardio-pulmonary function in male broilers that initially were reared together at normal brooding temperatures and then were randomly assigned to chambers maintained at 28 C (warm group) or 16 C (cool group). Cardio-pulmonary evaluations were conducted between 35 and 42 d of age. The groups initially did not differ in body weight, right:total ventricular weight ratio, respiratory rate, heart rate, total peripheral resistance, or pulmonary vascular resistance, nor did their arterial blood gas values differ for the partial pressure of carbon dioxide, bicarbonate concentration, or hydrogen ion concentration. When compared with the warm group, the cool group had heavier total ventricular weights and higher values for pulmonary arterial pressure, cardiac output, stroke volume, mean systemic arterial pressure, and hematocrit and a marginally lower (P = 0.06) partial pressure of oxygen. Inhaling 100% O2 for 20 min caused equivalent increases in the arterial partial pressure of oxygen (> or =388 mm Hg) and the percentage saturation of hemoglobin with oxygen (99.9%) in both groups. The respiratory rate was reduced and total peripheral resistance in both groups was increased; the pulmonary arterial pressure, cardiac output, and heart rate in the cool group were also reduced. Cool temperatures contributed to the increase in pulmonary arterial pressure primarily by increasing the metabolic demand for oxygen, as reflected by incipient hypoxemia (reduced blood oxygen and elevated hematocrit), generalized ventricular hypertrophy, and an elevated cardiac output. It was the elevated cardiac output rather than hypoxemic pulmonary vasoconstriction that increased the pulmonary arterial pressure in the cool group when compared with the warm group.

We evaluated the influence of the percentage saturation of hemoglobin with oxygen (HbO2) on the pulmonary arterial pressure in normal and preascitic (hypoxemic) broilers breathing ambient air or 100% O2. In Experiment 1, unanesthetized preascitic broilers (right:total ventricular weight ratios [RV:TV] = 0.32+/-0.02) breathing ambient air had initial values of 67% for HbO2 and 32 mm Hg for pulmonary arterial pressure. The HbO2 increased to > or =96.6% during inhalation of 100% O2; however, pulmonary arterial pressure was not reduced. In Experiment 2, anesthetized normal (RV:TV = 0.23; HbO2 = 88%) and preascitic broilers (RV:TV = 0.28; HbO2 = 76%) were compared. The groups did not differ in body weight or respiratory rate, but preascitic broilers had lower values for mean arterial pressure, total peripheral resistance, and partial pressure of O2 in arterial blood and had higher values for pulmonary arterial pressure. Inhaling 100% O2 increased HbO2 to 99.9% in both groups; however, pulmonary arterial pressure remained higher in preascitic than in normal broilers, and the pulmonary vascular resistance was not reduced during 100% O2 inhalation. Cardiac output was higher in preascitic than in normal broilers before and after, but not during, 100% O2 inhalation. Mean arterial pressure and total peripheral resistance increased in the preascitic but not in the normal group during 100% O2 inhalation. Low coefficients of determination (R2) were obtained for linear regression comparisons of HbO2 vs. pulmonary arterial pressure in both experiments. Overall, acute reversal of the systemic hypoxemia in preascitic broilers had little direct impact on pulmonary hypertension, providing no evidence of hypoxemic or hypoxic pulmonary vasoconstriction. Instead, acute reversal of the systemic hypoxemia primarily increased the total peripheral resistance and normalized the mean arterial pressure and cardiac output. A sustained reduction in cardiac output theoretically should attenuate pulmonary hypertension, but this was not observed because of the overriding influence of sustained pulmonary vascular resistance.

Acutely tightening a snare around one pulmonary artery previously was shown to trigger a reversible ventilation-perfusion (V/Q) mismatch in broilers, as reflected by decreases in the partial pressure of oxygen in arterial blood (hypoxemia), accompanied by increases in the hydrogen ion concentration (acidosis) and partial pressure of carbon dioxide (hypercapnia). In the present study, snares were loosely implanted around the right pulmonary artery and the right extrapulmonary primary bronchus in anesthetized male broilers. These snares were tightened and released independently and then simultaneously to evaluate the possibility that directing the entire respiratory minute volume toward the left lung might attenuate the V/Q mismatch caused by forcing the entire cardiac output (CO) through the left lung. Fully reversible arterial blood hypoxemia, acidosis, and hypercapnia occurred when either snare was tightened independently. Presumably, tightening the bronchial snare restricted ventilation but not blood flow to the right lung, thereby permitting blood to perfuse poorly ventilated gas exchange surfaces. Simultaneously tightening both snares triggered arterial blood hypoxemia, acidosis, and hypercapnia similar to or greater in magnitude than the responses obtained by tightening the pulmonary artery snare independently. Tightening either snare independently or both snares simultaneously caused pulmonary arterial pressure to increase (pulmonary hypertension), and permanent obstruction of one bronchus in a separate experiment caused an increase in the right:total ventricular weight ratio, which is indicative of chronic pulmonary hypertension. The mean systemic arterial pressure decreased when the pulmonary artery snare was tightened independently or in combination with the bronchial snare, but not when the bronchial snare was tightened independently. The respiratory rate increased and the heart rate decreased when the pulmonary artery snare was tightened independently, but not when the bronchial snare was tightened independently or in combination with the pulmonary artery snare. These results demonstrate that the V/Q mismatch caused by forcing all the CO to perfuse one lung cannot be attenuated by simultaneously directing the entire respiratory minute volume toward the same lung.