McGeer J C, Eddy F B
Department of Biological Science, University of Dundee, United Kingdom.
Physiol Zool. 1998 Mar-Apr;71(2):179-90. doi: 10.1086/515895.
Rainbow trout exposed to unbuffered water of pH 10.5 initially showed significant increases in blood pH, plasma cortisol and glucose, partial pressure of NH3 (PNH3), NH4+, and HCO3- values as well as loss of plasma Cl-, reduced partial pressure of CO2 (PCO2), and inhibition of total ammonia excretion rate. After the first day, fish resisted further change, and new levels were established (for blood pH and plasma PCO2 and PNH3 levels) or imbalances corrected, either partially (for total ammonia excretion) or completely (for plasma Cl-, HCO3-, cortisol, and glucose values). During the 7-d exposure, 80% of fish in unbuffered water survived, but in buffered water (0.75 mmol L(-1) glycine-buffered KOH at pH 10.5), survival was only 50% after 3 d, and ion regulatory failure was evident. Fish in buffered and unbuffered alkaline waters had similar total ammonia excretion rates, which suggests that glycine-buffered KOH was not sufficient to significantly reduce gill boundary layer acidification. After 7 d in unbuffered alkaline water, 30% of total ammonia excretion was linked with an amiloride-sensitive (0.1 mmol L(-1)) Na+ uptake mechanism. Treatment of alkaline-exposed trout with waterborne acetazolamide (1.5 mmol L(-1)) indicated that gill boundary layer H+ production, through hydration of CO2, had a role in excretion of total ammonia. Exposure to 4-acetamino-4'-isothiocyantostilbene-2,2'-disulphonic acid (SITS; 0.1 mmol L(-1)) following 24-h exposure to unbuffered alkaline water resulted in increased plasma HCO3- and lowered plasma Cl- concentrations, indicating the role of branchial Cl-/HCO3- exchange in regaining Cl- lost and eliminating the HCO3- accumulated during exposure to alkaline water.
暴露于pH值为10.5的未缓冲水中的虹鳟鱼，最初血液pH值、血浆皮质醇和葡萄糖、NH3分压（PNH3）、NH4+和HCO3-值显著升高，同时血浆Cl-流失、CO2分压（PCO2）降低，总氨排泄率受到抑制。第一天后，鱼抵抗了进一步的变化，并建立了新的水平（血液pH值、血浆PCO2和PNH3水平），或者部分（总氨排泄）或完全（血浆Cl-、HCO3-、皮质醇和葡萄糖值）纠正了失衡。在7天的暴露期间，未缓冲水中80%的鱼存活，但在缓冲水（pH值为10.5的0.75 mmol L(-1)甘氨酸缓冲KOH）中，3天后存活率仅为50%，离子调节失败明显。缓冲和未缓冲碱性水中的鱼总氨排泄率相似，这表明甘氨酸缓冲KOH不足以显著降低鳃边界层酸化。在未缓冲碱性水中暴露7天后，总氨排泄的30%与氨氯吡咪敏感（0.1 mmol L(-1)）的Na+摄取机制有关。用水性乙酰唑胺（1.5 mmol L(-1)）处理碱性暴露的鳟鱼表明，通过CO2水合作用产生的鳃边界层H+在总氨排泄中起作用。在暴露于未缓冲碱性水24小时后，再暴露于4-乙酰氨基-4'-异硫氰基芪-2,2'-二磺酸（SITS；0.1 mmol L(-1)）导致血浆HCO3-升高，血浆Cl-浓度降低，表明鳃Cl-/HCO3-交换在恢复暴露于碱性水期间流失的Cl-和消除积累的HCO3-中的作用。
