Pulmonary arterial hypertension (PAH) syndrome in broilers - also known as ascites syndrome and pulmonary hypertension syndrome - can be attributed to imbalances between cardiac output and the anatomical capacity of the pulmonary vasculature to accommodate ever-increasing rates of blood flow, as well as to an inappropriately elevated tone (degree of constriction) maintained by the pulmonary arterioles.

According to R.F. Wideman and colleagues at the University of Arkansas in their review paper in Poultry Science, comparisons of PAH-susceptible and PAH-resistant broilers do not consistently reveal differences in cardiac output but PAH-susceptible broilers consistently have higher pulmonary arterial pressures and pulmonary vascular resistances than PAH-resistant broilers.

Efforts clarify the causes of excessive pulmonary vascular resistance have focused on evaluating the roles of chemical mediators of vasoconstriction and vasodilation, as well as on pathological (structural) changes occurring within the pulmonary arterioles (e.g. vascular remodeling and pathology) during the pathogenesis of PAH.

The objectives of the Fayetteville review were to:

1. summarise the pathophysiological progression initiated by the onset of pulmonary hypertension and culminating in terminal ascites
2. review recent information regarding the factors contributing to excessively elevated resistance to blood flow through the lungs
3. assess the role of the immune system during the pathogenesis of PAH, and
4. present new insights into the genetic basis of PAH.

The University of Arkansas group reports that cumulative evidence attributes the elevated pulmonary vascular resistance in PAH-susceptible broilers to an anatomically inadequate pulmonary vascular capacity, to excessive vascular tone reflecting the dominance of pulmonary vasoconstrictors over vasodilators, and to vascular pathology elicited by excessive haemodynamic stress.

Emerging evidence also demonstrates that the pathogenesis of PAH includes characteristics of an inflammatory/autoimmune disease involving multifactorial genetic, environmental and immune system components.

Pulmonary arterial hypertension susceptibility appears to be multigenic and may be manifested in aberrant stress sensitivity, function and regulation of pulmonary vascular tissue components, as well as aberrant activities of innate and adaptive immune system components.

Major genetic influences and high heritabilities for PAH susceptibility have been demonstrated by numerous investigators.

Selection pressures rigorously focused to challenge the pulmonary vascular capacity readily expose the genetic basis for spontaneous PAH in broilers.

Chromosomal mapping continues to identify regions associated with ascites susceptibility, and candidate genes have been identified.

Wideman and colleagues conclude that ongoing immunological and genomic investigations are likely to continue generating important new knowledge regarding the fundamental biological bases for the PAH/ascites syndrome.

Reference

Wideman R.F., D.D. Rhoads, G.F. Erf and N.B. Anthony. 2013. Pulmonary arterial hypertension (ascites syndrome) in broilers: A review. Poult. Sci. 92(1):64-83. doi: 10.3382/ps.2012-02745

You can view the full report by clicking here.

Find out more information on ascites by clicking here.

February 2013