THE MECHANISMS OF ACID--BASE AND IONOREGULATION IN FRESHWATER RAINBOW TROUT DURING ENVIRONMENTAL HYPEROXIA AND SUBSEQUENT NORMOXIA. I. EXTRA- AND INTRACELLULAR ACID--BASE STATUS THE HELVE HOBE*, CHRIS M. WOOD and MICHELE G. WHEATLY**

Al~tmct. The extracellular acid-base status of the freshwater rainbow trout (Salmo gairdneri) was continuously monitored during 24 h normoxia (Pxo: = 120-150 tort; control), 72 h hyperoxia (Pioz = 500-600 tort) and 24 h return to normoxia. Hyperoxla induced a marked respiratory acidosis (ApHe = -0.23 unit) due to a 3-fold elevation in arterial CO 2 tension which was completely compensated over 72 h by a comparable rise in plasma bicarbonate, reflecting effective removal of acidic equivalents from the ECF. Upon return to normoxia, arterial CO 2 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 ECF occurred more rapidly than the original removal. lntracellular 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 p i l e p H i gradient of ca. 0.5 during normoxia, and underwent identical changes during hyperoxia, lntraceilular 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 pile regulation did not occur at the expense of pHi regulation. The ultimate restoration of both pile and ph i during hyperoxia must have occurred v/a kidney or gills.