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A pulmonary artery clamp model for inducing pulmonary hypertension syndrome (ascites) in broilers
1Department of Poultry Science, University of Arkansas, Fayetteville 72701, USA.
Insights
A primary increase in pulmonary vascular resistance directly induces pulmonary hypertension syndrome (PHS) and ascites in broiler chicks. This finding establishes a causal link between elevated pulmonary vascular resistance and PHS development.
Area of Science:
- Cardiovascular Physiology
- Avian Pathophysiology
- Pulmonary Hypertension Research
Background:
- Pulmonary hypertension syndrome (PHS), characterized by ascites, is a significant concern in broiler production.
- The precise initiating factors of PHS remain incompletely understood.
- Previous research suggested multifactorial causes, but a direct link to pulmonary vascular resistance was not established.
Purpose of the Study:
- To test the hypothesis that a primary increase in pulmonary vascular resistance can initiate the pathophysiological progression leading to PHS.
- To establish a direct causal relationship between elevated pulmonary vascular resistance and the development of ascites in broiler chickens.
Main Methods:
- Surgically clamping the left pulmonary artery in male broiler chicks (15-19 days of age) to increase pulmonary vascular resistance.
- Utilizing control (sham-operated) groups and groups with partial pulmonary artery occlusion for comparison.
- Assessing PHS incidence, right:total ventricular weight ratios (right ventricular hypertrophy), electrocardiogram lead II R-S wave amplitudes, hemoglobin oxygen saturation, and hematocrit levels.
Main Results:
- A high incidence of PHS (90% and 68%) was observed in broilers with a surgically clamped left pulmonary artery.
- Control and partially occluded groups showed significantly lower PHS incidence (8% and 0%).
- Pulmonary hypertension (right ventricular hypertrophy) and systemic hypoxemia (low oxygen saturation, elevated hematocrit) were characteristic of broilers that developed ascites.
Conclusions:
- This study provides the first direct evidence that PHS (ascites) can be induced by a primary increase in pulmonary vascular resistance.
- The broiler lung's capacity to oxygenate blood may be compromised when subjected to increased cardiac output and elevated pulmonary arterial pressure.
- Findings suggest that managing pulmonary vascular resistance is critical for preventing PHS in broiler chickens.
Abstract:
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 (PHS, 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.