Seawater carbonate chemistry and physiological performance parameters of Carcinus maenas under respective incubation conditions@en

Ocean acidification causes an accumulation of CO2 in marine organisms and leads to shifts in acid-base parameters. Acid-base regulation in gill breathers involves a net increase of internal bicarbonate levels through transmembrane ion exchange with the surrounding water. Successful maintenance of body fluid pH depends on the functional capacity of ion-exchange mechanisms and associated energy budget. For a detailed understanding of the dependence of acid-base regulation on water parameters, we investigated the physiological responses of the shore crab Carcinus maenas to 4 weeks of ocean acidification [OA, P(CO2)w = 1800 µatm], at variable water bicarbonate levels, paralleled by changes in water pH. Cardiovascular performance was determined together with extra-(pHe) and intracellular pH (pHi), oxygen consumption, haemolymph CO2 parameters, and ion composition. High water P(CO2) caused haemolymph P(CO2) to rise, but pHe and pHi remained constant due to increased haemolymph and cellular [HCO3-]. This process was effective even under reduced seawater pH and bicarbonate concentrations. While extracellular cation concentrations increased throughout, anion levels remained constant or decreased. Despite similar levels of haemolymph pH and ion concentrations under OA, metabolic rates, and haemolymph flow were significantly depressed by 40 and 30%, respectively, when OA was combined with reduced seawater [HCO3-] and pH. Our findings suggest an influence of water bicarbonate levels on metabolic rates as well as on correlations between blood flow and pHe. This previously unknown phenomenon should direct attention to pathways of acid-base regulation and their potential feedback on whole-animal energy demand, in relation with changing seawater carbonate parameters.

海洋酸化（Ocean Acidification, OA）会导致海洋生物体内二氧化碳蓄积，并引发酸碱参数偏移。鳃呼吸生物的酸碱调节（acid-base regulation）依赖于与周围水体进行跨膜离子交换（transmembrane ion exchange），从而实现体内碳酸氢盐水平的净升高。体液pH的稳定维持取决于离子交换机制的功能能力与相关能量收支。为深入理解酸碱调节对水体参数的依赖关系，本研究针对滨蟹（Carcinus maenas）开展了为期4周的海洋酸化胁迫实验，实验设置了可变的水体碳酸氢盐水平，并同步伴随水体pH变化，其中海洋酸化组的海水二氧化碳分压P(CO₂)w=1800 µatm。本研究测定了其心血管功能、细胞外pH（extracellular pH, pHe）与细胞内pH（intracellular pH, pHi）、耗氧量（oxygen consumption）、血淋巴（haemolymph）二氧化碳参数及离子组成。高海水二氧化碳分压会导致血淋巴二氧化碳分压升高，但由于血淋巴与细胞内碳酸氢盐浓度[HCO₃⁻]升高，细胞外pH与细胞内pH得以保持稳定。该调节过程在降低的海水pH与碳酸氢盐浓度条件下依然有效。细胞外阳离子浓度整体升高，而阴离子水平则保持稳定或有所下降。尽管在海洋酸化胁迫下血淋巴pH与离子浓度维持稳定，但当海洋酸化与降低的海水碳酸氢盐浓度及pH共同作用时，生物的代谢速率与血淋巴流量分别显著降低了40%与30%。本研究结果表明，水体碳酸氢盐水平会影响代谢速率以及血淋巴流量与细胞外pH之间的相关性。这一此前未被发现的现象，应促使学界关注酸碱调节通路及其对整个生物体能量需求的潜在反馈，该反馈与海水碳酸盐参数的变化密切相关。