Pathophysiology of heart/lung disorders: pulmonary hypertension syndrome in broiler chickens

Pulmonary hypertension syndrome (PHS, ascites) in broiler chickens provides an outstanding example of the pathophysiological interplay between the lungs and heart. Recent research has confirmed the hypothesis that PHS susceptible broilers have an inherent potential to outgrow their pulmonary vascular capacity. Definitive proof that pulmonary hypertension (PH) is initiated as a consequence of an excessive pulmonary arterial resistance was obtained through measurements of pulmonary wedge pressures. Definitive proof that a pulmonary diffusion limitation causes the hypoxaemia characteristic of susceptible broilers was demonstrated by the rapid return to full arterial blood oxygenation in pre-ascitic broilers when they were provided with 100% oxygen to breathe. Experiments involving acute and chronic unilateral pulmonary occlusion provided definitive proof that the entire pathogenesis of PHS can be replicated by reducing the pulmonary vascular capacity. These experiments conclusively demonstrate that the resistance of broilers to PHS depends upon the capacity of their pulmonary vasculature to accept the requisite cardiac output at blood flow rates and pressures sufficiently low to avoid triggering PH and systemic hypoxaemia. The chronic unilateral pulmonary artery occlusion technique was successfully applied to develop a broiler line that is highly resistant to PHS induced by fast growth and exposure to rigorous cool temperatures, demonstrating for the first time that a dominant gene codes for a highly significant proportion of the PHS susceptibility. We now possess the knowledge necessary to create broiler lines capable of maintaining extremely rapid growth under rigorous field conditions while retaining very low susceptibility to PHS.

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