Replication Data for: Taurine efflux counters the hydrodynamic impact of anaerobic metabolism to protect cardiorespiratory function under acute thermal stress in brook char (Salvelinus fontinalis)

Upper thermal tolerance may be limited by convective oxygen transport in fish, but the mechanisms constraining heart function remain elusive. The activation of anaerobic metabolism imposes an osmotic stress on cardiomyocytes at high temperatures that must be countered to prevent swelling and cardiac dysfunction. We tested the hypothesis that cardiac taurine efflux is required to counter the osmotic impact of anaerobic end product accumulation in brook char, Salvelinus fontinalis. Fish were fed a diet enriched in β-alanine, a competitive inhibitor of the taurine transporter, to induce taurine deficiency and inhibit transporter function. In vivo, stroke volume increased by 60% and cardiac output doubled in control fish during a 2 °C h-1 thermal ramp. Stroke volume was temperature-insensitive in taurine deficient (TD) fish so cardiac output was 30% lower at high temperatures. The thermal sensitivity of aerobic metabolism did not
differ, and lactate accumulated to a similar degree in both diet treatment groups, indicating that taurine deficiency does not impact energy metabolism. Heart taurine efflux was absent and ventricular muscle osmolality was 40 mOsmol kg-1 22 higher in TD brook char following thermal stress. Swelling and decreased ventricular compliance likely impair diastolic filling to constrain stroke volume in TD fish. The adrenaline sensitivity of cardiac contractility and the regulation of intracellular pH in brain and liver were also impacted in TD brook char. Taurine efflux appears necessary to counteract the hydrodynamic impact of activating anaerobic metabolism and this process may limit heart function under acute thermal stress.

鱼类的高温耐受上限可能受对流氧运输（convective oxygen transport）限制，但制约心脏功能的机制仍不明朗。高温下无氧代谢（anaerobic metabolism）的激活会对心肌细胞（cardiomyocytes）造成渗透压应激（osmotic stress），必须对此进行拮抗以避免细胞肿胀与心脏功能障碍。我们验证了这一假说：溪红点鲑（*Salvelinus fontinalis*）体内的心脏牛磺酸外流可拮抗无氧代谢终产物积累带来的渗透压影响。实验中，我们给溪红点鲑投喂富含β-丙氨酸（β-alanine，牛磺酸转运体（taurine transporter）的竞争性抑制剂）的饲料，以诱导牛磺酸缺乏（taurine deficiency, TD）并抑制转运体功能。在活体实验中，热梯度升温速率为2°C·h⁻¹时，对照组溪红点鲑的每搏输出量（stroke volume）提升60%，心输出量（cardiac output）翻倍。而牛磺酸缺乏组溪红点鲑的每搏输出量不受温度调控，因此高温下心输出量较对照组低30%。两组饲料处理组的有氧代谢（aerobic metabolism）热敏感性无差异，乳酸（lactate）积累水平也相近，表明牛磺酸缺乏并未影响能量代谢。热应激后，牛磺酸缺乏组溪红点鲑的心脏牛磺酸外流消失，心室肌渗透压（ventricular muscle osmolality）较对照组高40 mOsmol·kg⁻¹。细胞肿胀与心室顺应性（ventricular compliance）下降可能损害舒张充盈（diastolic filling），进而限制牛磺酸缺乏组溪红点鲑的每搏输出量。牛磺酸缺乏组溪红点鲑的心脏收缩力对肾上腺素（adrenaline）的敏感性，以及脑、肝脏的细胞内pH（intracellular pH）调控也受到了影响。综上，牛磺酸外流似乎是拮抗无氧代谢激活带来的流体动力学影响所必需的，这一过程可能在急性热应激下限制心脏功能。