“…Increases in the pulmonary arterial pressure theoretically can be attributed to increases in cardiac output as well as to increases in the resistance to blood flow through the pulmonary vasculature Wideman, 2000;Wideman et al, 2007; Figure 1A). Fast growth, full-feeding, acclimation to cool environmental temperatures, heat stress, hypoxemia, hypercapnia, and metabolic acidosis all clearly contribute to the pathogenesis of pulmonary hypertension in broilers by increasing the cardiac output, either directly by increasing the metabolic demand for O 2 , or indirectly by dilating the systemic arterioles and thereby increasing venous return (Peacock et al, 1989;Reeves et al, 1991;Owen et al, 1994;Fedde et al, 1998;Wideman et al, 1998aWideman et al, ,c, 1999aWideman et al, ,b, 2000Wideman et al, , 2003aWideman, 1999;). 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 compared with PAH-resistant broilers Wideman, 2001, 2006c;Wideman et al, , 2006Wideman et al, , 2007Bowen et al, 2006a;Lorenzoni et al, 2008).…”