CHRONIC UNILATERAL OCCLUSION OF AN EXTRAPULMONARY PRIMARY BRONCHUS INDUCES PULMONARY-HYPERTENSION SYNDROME (ASCITES) IN MALE AND FEMALE BROILERS

Previously, it was demonstrated that acute (4 min) and chronic (12 d) occlusion of an extrapulmonary primary bronchus triggers pulmonary hyp ertension but not pulmonary hypertension syndrome (PHS, ascites) in br oilers. The present study was conducted to determine whether a more pr olonged period of bronchus occlusion causes PHS similar to that induce d by clamping one pulmonary artery. Male and female broiler chicks, 14 to 18 d old, were anesthetized, the thoracic inlet was opened, and a silver clip was positioned to fully obstruct the left extrapulmonary p rimary bronchus (BRONCHUS CLAMP group) or the left pulmonary artery (P A-CLAMP group). Sham-operated chicks were anesthetized and the thoraci c inlet was opened; however, neither the pulmonary artery nor the bron chus was clamped (SHAM group). An electrocardiogram (EGG) was obtained whenever clinical ascites became apparent in individual broilers, or prior to the final necropsy for broilers surviving to the end (Day 36) of the experiment. The right:total ventricular weight ratio (RV:TV) w as evaluated as an index of pulmonary arterial pressure. Early pest-su rgical mortality (up to 21 d of age) was higher in the PA-CLAMP group (27% for males and females combined) than in the BRONCHUS CLAMP (10%) and SHAM (2%) groups. Cumulative ascites mortality (Days 22 to 36) als o was higher in the PA-CLAMP group (86% for males, 77% for females) th an in the BRONCHUS CLAMP (69% for males, 41% for females) and SHAM (23 % for males, 0% for females) groups. Ascitic birds in all treatment gr oups had higher RV:TV ratios and more negative ECG Lead II S-wave ampl itudes than nonascitic birds, reflecting the right ventricular hypertr ophy and generalized ventricular dilation typically associated with PH S. These results demonstrate that unilateral bronchus occlusion is an effective experimental model for triggering ascites at a lower inciden ce than that obtained by occluding one pulmonary artery. Following the onset of pulmonary hypertension, the pathophysiological progression l eading to ascites appears to be similar for broilers with either unila teral bronchus or pulmonary artery occlusion.