Shingles A, McKenzie D J, Taylor E W, Moretti A, Butler P J, Ceradini S
School of Biosciences, University of Birmingham, Birmingham, B15 2TT, UK.
J Exp Biol. 2001 Aug;204(Pt 15):2691-8. doi: 10.1242/jeb.204.15.2691.
Adult trout Oncorhynchus mykiss fitted with a dorsal aortic catheter were exposed to 288+/-15 micromol l(-1) (mean +/- S.E.M.) total ammonia for 24h in water at a pH of 8.39+/-0.02, while swimming at a speed equivalent to 0.75 bodylengths s(-1) (BLs(-1)) in a Brett-type tunnel respirometer. The fish were then exposed to stepwise increments in swimming speed (0.25 BLs(-1) every 30 min) until exhaustion. Measurements of oxygen uptake (M(O2)) and plasma total ammonia levels and pH were made at each speed. Control trout were treated identically but without exposure to ammonia. Ammonia exposure caused an increase in plasma total ammonia level to 436+/-34 micromol l(-1), compared to 183+/-30 micromol l(-1)in control animals (N=6). A significant reduction in total plasma ammonia level was found in both groups during exercise, despite a large negative concentration gradient in those exposed to an elevated concentration of ammonia in water, which may indicate an active excretory process. The overall increase in plasma ammonia levels in exposed trout was associated with a significant reduction in critical swimming speed (U(crit)) to 1.61+/-0.17BL s(-1) from 2.23+/-0.15BL s(-1) in control animals. Ammonia-exposed trout had a significantly higher maintenance metabolic rate (MMR) than control fish, when estimated as the y-intercept of the relationship between swimming speed and M(O2). Active metabolic rate (AMR, maximum M(O2) as measured at U(crit)) was significantly lower in ammonia-exposed animals, leading to a profound reduction in factorial aerobic scope (AMR/MMR). Reduced U(crit) was also linked to a reduction in maximum tailbeat frequency. Calculation of membrane potentials (E(M)) in the white muscle of fish swum to U(crit) revealed a significant partial depolarisation of white muscle in ammonia-exposed fish. This may have prevented white muscle recruitment and contributed to the reduced maximum tailbeat frequency and overall impairment of swimming performance in the ammonia-exposed fish.
将背主动脉导管植入的成年虹鳟(Oncorhynchus mykiss)在pH值为8.39±0.02的水中,以相当于0.75体长每秒(BL s⁻¹)的速度在布雷特型隧道呼吸仪中游泳时,暴露于288±15微摩尔每升(μmol l⁻¹)(平均值±标准误)的总氨环境中24小时。然后,让鱼的游泳速度逐步增加(每30分钟增加0.25 BL s⁻¹),直至精疲力竭。在每个速度下测量氧气摄取量(M(O₂))、血浆总氨水平和pH值。对照虹鳟接受相同处理,但不暴露于氨环境。氨暴露使血浆总氨水平升至436±34微摩尔每升,而对照动物为183±30微摩尔每升(N = 6)。尽管暴露于水中氨浓度升高的鱼体内存在很大的负浓度梯度,但两组在运动期间血浆总氨水平均显著降低,这可能表明存在活跃的排泄过程。暴露于氨的虹鳟血浆氨水平的总体升高与临界游泳速度(U(crit))从对照动物的2.23±0.15 BL s⁻¹显著降至1.61±0.17 BL s⁻¹有关。当以游泳速度与M(O₂)之间关系的y轴截距估算时,暴露于氨的虹鳟的维持代谢率(MMR)显著高于对照鱼。暴露于氨的动物的活跃代谢率(AMR,在U(crit)时测量的最大M(O₂))显著较低,导致有氧范围系数(AMR/MMR)大幅降低。U(crit)降低还与最大尾鳍摆动频率降低有关。对游至U(crit)的鱼的白色肌肉进行膜电位(E(M))计算发现,暴露于氨的鱼的白色肌肉存在显著的部分去极化。这可能阻止了白色肌肉的募集,并导致暴露于氨的鱼的最大尾鳍摆动频率降低和游泳性能整体受损。