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

Two experiments were conducted to test the hypothesis that a primary increase in pulmonary vascular resistance can initiate a pathophysiological progression leading to pulmonary hypertension syndrome (PI-IS, ascites). Pulmonary vascular resistance was increased by surgically clamping 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 68% incidence of PHS in Experiment 2. The incidence of PHS was 8% for control or sham-operated broilers in Experiment 1, whereas in Experiment 2 no (0%) PHS occurred in sham-operated broilers or in individuals with a pulmonary artery that only was partially occluded. Broilers with a fully occluded left pulmonary artery developed pulmonary hypertension, as demonstrated by increased right:total ventricular weight ratios (right ventricular hypertrophy) and by increased electrocardiogram lead II R-S wave amplitudes (generalized ventricular dilation and hypertrophy). Forcing the entire cardiac output through the right lung resulted in a lower percentage saturation of hemoglobin with oxygen and an elevated hematocrit, reflecting generalized systemic hypoxemia. Pulmonary hypertension and hypoxemia also were specifically characteristic of all birds that developed ascites, regardless of treatment group. These observations demonstrate for the first time that PHS (ascites) can be directly induced by a primary increase in pulmonary vascular resistance. The observed changes in percentage saturation of hemoglobin with oxygen suggest that the lungs of broilers may be unable to efficiently oxygenate the blood when forced to receive an increased cardiac output at an elevated pulmonary arterial pressure.