Exposure of rainbow trout to environmental hyperoxia (Plo2 ∼ 530 Torr) resulted in an extracellular respiratory acidosis which was fully compensated by 72 h; return to normoxia (Plo2 ∼ 145 Torr) at this time induced a metabolic alkalosis which was corrected by 24 h. Intracellular pHi ([14C]DMO method), fluid volumes [3H]PEG-4000 method), and electrolytes were monitored. Environmental hypercapnia (Plco2 ∼ 6.5 Torr) was employed to confirm that intracellular responses were specific to respiratory acidosis. Gill pHi did not change during respiratory acidosis despite a very low non-HCO3 buffer capacity, but gill ICFV decreased markedly. A large loss of gill intracellular [Cl ]i in excess of [Na+]i, combined with a substantial gain in [K+]i, contributed to gill pHi regulation by raising branchial [SID]i. In weakly buffered brain tissue, active adjustment of pHi started within 3 h, but two well buffered tissues, RBC and white muscle, exhibited compounding metabolic acidoses during the first 12-24 h. The muscle response was associated with small increases in ICFV and [Cl ]i, and a large decrease in [K+]i which reduced muscle [SID]i. We hypothesize that this initial export of K+ and basic equivalents served to regulate pH in more critical compartments (e.g. gills, brain) at the expense of muscle acidosis. By 48 h, pHi restoration in all tissues was complete, in advance of pHe regulation (72 h). Return to normoxia at 72 h elevated muscle, brain, and gill pHi, but there was no evidence of a comparable 'altruistic' role of muscle during this metabolic alkalosis. Regulation of pHi was complete by 24 h recovery, accompanied by partial or complete restoration of intracellular ions and fluid volumes.
- Acid-base status, intracellular, hyperoxia (trout)
- Electrolytes, intracellular Na, K
- Fish, rainbow trout
- Hyperoxia, acid-base status (trout)
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine