Taurine, cardiopulmonary hemodynamics, and pulmonary hypertension syndromein broilers

Previous studies have suggested cardiac taurine is released into the plasma in response to hypoxemia (low blood oxygen levels) during the pathogenesis of pulmonary hypertension syndrome (PHS, ascites). In the present study, b roilers reared under cool temperature conditions (16 C) were provided tap w ater (control group), tap water supplemented with taurine, or tap water sup plemented with the taurine transport antagonist beta -alanine. When compare d with control values, taurine supplementation consistently elevated free t aurine concentrations in the plasma but not in cardiac tissues, whereas bet a -alanine supplementation consistently reduced free taurine concentrations in cardiac tissues but not in the plasma. Neither the incidence of PHS nor specific predictors of PHS susceptibility (electrocardiogram Lead II S-wav e amplitude, % saturation of hemoglobin with oxygen, heart rate, right to t otal ventricular weight ratio) were affected by taurine or beta -alanine su pplementation. Cardiopulmonary hemodynamic evaluations were conducted to co mpare control and beta -alanine supplemented broilers breathing room air or air containing 12% oxygen (low oxygen challenge). While breathing room air , the beta -alanine-supplemented broilers had higher baseline values for ca rdiac output (186.2 vs. 146.9 mL/min/kg BW) and pulmonary arterial pressure (27.4 vs. 22.4 mm Hg), similar values for mean systemic arterial pressure (100 vs. 104 mm Hg) and pulmonary vascular resistance (0.062 vs. 0.064 resi stance units), and lower values for total peripheral resistance (0.228 vs. 0.296 resistance-units) when compared with control broilers breathing room air. During low oxygen challenges, the beta -alanine-supplemented broilers exhibited larger reductions in cardiac output, mean systemic arterial press ure, and pulmonary arterial pressure and greater increases in pulmonary vas cular resistance than control broilers. These observations indicate that be ta -alanine-supplemented broilers breathing room air had a higher systemic demand for oxygen as evidenced by their lower total peripheral resistance ( systemic vasodilation) and had a capacity sufficient to pump a higher cardi ac output and, thereby, maintain a similar mean systemic arterial pressure when compared with control broilers. However, cardiac function rapidly dete riorated in beta -alanine-supplemented broilers during low oxygen challenge s leading to substantially greater reductions in cardiac output, stroke vol ume, and mean systemic arterial pressure when compared with control broiler s. Concurrent changes in pulmonary arterial pressure within the beta -alani ne group reflect interactions between cardiac output and pulmonary vascular resistance. Overall, depleting cardiac taurine did not appear to initiate PHS, but systemic hypoxemia developing during the mid- to late-pathogenesis of PHS may expose and incipient cardiac weakness attributable to depleted taurine reserves.