Wood C M, Wheatly M G, Hobe H
Respir Physiol. 1984 Feb;55(2):175-92. doi: 10.1016/0034-5687(84)90021-5.
Fluxes of both acidic equivalents (JH+net) and electrolytes across the gills were continuously monitored in the freshwater rainbow trout (Salmo gairdneri) during 24 h normoxia (PIO2 = 120-150 torr; control), 72 h hyperoxia (PIO2 = 500-600 torr), and 24 h return to normoxia. A highly negative JH+net (i.e., excretion) was responsible for over 90% of the compensation of respiratory acidosis induced by hyperoxia in the whole animal. Similarly, a highly positive JH+net (i.e., uptake) accounted for virtually all the compensation of metabolic alkalosis induced by normoxic recovery. Hyperoxia was associated with a small net gain of Na+ and large net losses of Cl- at the gills, while normoxic recovery was associated with large net losses of Na+ and net gains of Cl-, effects reflected in ECF composition. Unidirectional flux analyses with radiotracers (22Na, 36Cl) demonstrated that these net flux alterations resulted from rapid and complex changes in both influx and efflux components such that the difference between JNa+net and JCl-net was stoichiometrically equivalent to JH+net. The results support the concept that Na+ vs acidic equivalent (H+, NH+4) and Cl- vs basic equivalent (HCO-3, OH-) exchanges at the gill are dynamically adjusted in order to correct internal acid-base disturbances.
在24小时常氧(动脉血氧分压 = 120 - 150托;对照组)、72小时高氧(动脉血氧分压 = 500 - 600托)以及24小时恢复常氧期间,持续监测淡水虹鳟(虹鳟)鳃对酸性当量(JH⁺净通量)和电解质的通量。高度负的JH⁺净通量(即排泄)在整个动物体中对高氧诱导的呼吸性酸中毒的补偿作用超过90%。同样,高度正的JH⁺净通量(即摄取)几乎构成了常氧恢复诱导的代谢性碱中毒的所有补偿。高氧与鳃处Na⁺的少量净增加和Cl⁻的大量净损失相关,而常氧恢复与Na⁺的大量净损失和Cl⁻的净增加相关,这些效应反映在细胞外液组成中。用放射性示踪剂(²²Na、³⁶Cl)进行的单向通量分析表明,这些净通量变化是由流入和流出成分的快速而复杂的变化引起的,使得JNa⁺净通量和JCl⁻净通量之间的差异在化学计量上等同于JH⁺净通量。结果支持这样的概念,即鳃处的Na⁺与酸性当量(H⁺、NH₄⁺)以及Cl⁻与碱性当量(HCO₃⁻、OH⁻)的交换是动态调节的,以纠正体内酸碱紊乱。