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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Exposure of rainbow trout to environmental hyperoxia (PIO2 approximately 530 Torr) resulted in an extracellular respiratory acidosis which was fully compensated by 72 h; return to normoxia (PIO2 approximately 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 (PICO2 approximately 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.
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PMID:Intracellular acid-base responses to environmental hyperoxia and normoxic recovery in rainbow trout. 175 56

The extracellular acid-base status of the freshwater rainbow trout (Salmo gairdneri) was continuously monitored during 24 h normoxia (PIO2 = 120-150 torr; control), 72 h hyperoxia (PIO2 = 500-600 torr) and 24 h return to normoxia. Hyperoxia induced a marked respiratory acidosis (delta 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 equivalents 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 ECF 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. 0.5 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.
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PMID: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. 642 70