A PULMONARY-ARTERY CLAMP MODEL FOR INDUCING PULMONARY-HYPERTENSION SYNDROME (ASCITES) IN BROILERS

Two experiments were conducted to test the hypothesis that a primary i ncrease in pulmonary vascular resistance can initiate a pathophysiolog ical progression leading to pulmonary hypertension syndrome (PI-IS, as cites). Pulmonary vascular resistance was increased by surgically clam ping the left pulmonary artery when male broiler chicks were 15 to 19 d of age, resulting in a 90% incidence of PHS in Experiment 1, and a 6 8% incidence of PHS in Experiment 2. The incidence of PHS was 8% for c ontrol or sham-operated broilers in Experiment 1, whereas in Experimen t 2 no (0%) PHS occurred in sham-operated broilers or in individuals w ith a pulmonary artery that only was partially occluded. Broilers with a fully occluded left pulmonary artery developed pulmonary hypertensi on, as demonstrated by increased right:total ventricular weight ratios (right ventricular hypertrophy) and by increased electrocardiogram le ad II R-S wave amplitudes (generalized ventricular dilation and hypert rophy). Forcing the entire cardiac output through the right lung resul ted in a lower percentage saturation of hemoglobin with oxygen and an elevated hematocrit, reflecting generalized systemic hypoxemia. Pulmon ary hypertension and hypoxemia also were specifically characteristic o f all birds that developed ascites, regardless of treatment group. The se observations demonstrate for the first time that PHS (ascites) can be directly induced by a primary increase in pulmonary vascular resist ance. The observed changes in percentage saturation of hemoglobin with oxygen suggest that the lungs of broilers may be unable to efficientl y oxygenate the blood when forced to receive an increased cardiac outp ut at an elevated pulmonary arterial pressure.