Plasma taurine levels in broilers with pulmonary hypertension syndrome induced by unilateral pulmonary artery occlusion

Low plasma levels of taurine are associated with losses of cardiac sarcomer ic proteins, leading to heart failure in mammals. Recently, it was proposed that cardiac taurine depletion serves to defend the heart against injury c aused by regional ischemia in mammals. The role of taurine has not been wel l documented in broilers, particularly in relation to pulmonary hypertensio n syndrome (PHS; ascites). Three independent experiments evaluated plasma t aurine in male broilers by utilizing the following treatments: unoperated c ontrols (CONTROL; n = 10 in each experiment); sham operated (SHAM; n = 11, 12, and 10); or, unilaterally pulmonary artery clamped (PAC; n = 18, 29, an d 24) that did (PAC-ascites) or did not (PAC-normal) develop ascites within 12 d postsurgery. Plasma samples were collected 9 and 11 d postsurgery in Experiments 1 and 2, respectively, and 2 d before and 4, 8, and 12 d after surgery in:Experiment 3. Plasma taurine was analyzed by HPLC. Twelve days p ostsurgery, the birds were euthanatized, and ventricles were weighed for ca lculating the right:total ventricular weight ratio (RV:TV). The RV:TV of PA C birds (>0.35) consistently was higher (P < 0.01) than that of CONTROL and SHAM birds (<0.27 and 0.25, respectively). In Experiments 1 and 2, plasma taurine was higher (P < 0.05) in PAC-ascites (380 and 370 nmol/mL) than in SHAM broilers (183 and 186 nmol/mL), whereas CONTROL (262 and 278 nmol/mL) and PAC-normal (362 and 300 nmol/mL) broilers tended to have intermediate p lasma taurine levels. Ln Experiment 3, PAC birds had higher (P < 0.05) plas ma taurine at 8 and 12 d postsurgery when compared with:presurgery levels, whereas plasma taurine was unchanged over time in CONTROL and SHAM birds. T hese results suggest cardiac taurine may be released into the plasma as a p rotective mechanism in response to the induction of pulmonary hypertension, hypoxemia, and right-side heart failure, similar to the mechanism reported for protecting cardiac muscle from ischemia in mammals.