The mechanisms of acid-base and ionoregulation in the freshwater rainbow trout during environmental hyperoxia and subsequent normoxia. I. Extra- and intracellular acid-base status

The extracellular acid-base status of the freshwater rainbow trout (Salmo gairdneri) was continuously monitored during 24 h normoxia (PI_O2 = 120-150 torr; control), 72 h hyperoxia (PI_O2 = 500-600 torr) torr) and 24 h return to normoxia. Hyperoxia induced a marked respiratory acidosis (†pHe = -0.23 unit) due to a 3-fold elevation in arterial CO₂ tension which was completely compensated over 72 h by a comparable rise in plasma bicarbonate, reflecting effective removal of acidic equavalents from the ECF. Upon return to normoxia, arterial CO₂ tension rapidly returned to normal against a background of high plasma bicarbonate, provoking a metabolic alkalosis which was largely compensated by 24 h. This effective restoration of acidic equivalents in the EXF occurred more rapidly than the original removal. Intracellular acid-base status was measured during normoxia and after 72 h hyperoxia using the steady state distribution of ¹⁴C-DMO. The rate of ¹⁴C-DMO excretion was 0.479±0.048 (%DMO lost per hour) during normoxia, and significantly decreased with hyperoxia. A considerable overestimate of mean whole body pHi would have resulted had this not been taken into account. Whole body and white expaxial muscle were similar with a pHe - pHi gradient of ca during normoxia, and underwent identical changes during hyperoxia. Intracellular pH was completely compensated by 72 h hyperoxia as intracellular bicarbonate increased 4-fold. The overall net removal of acidic equivalents from the ICFV was approximately one half that from the ECFV, but pHe regulation did not occur at the expense of pHi regulation. The ultimate restoration of both pHe and pHi during hyperoxia must have occurred via kidney or gills.