Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of exposure to high partial pressures of oxygen on transtracheal influx of chloramphenicol (Chlor) were examined using in vitro perfusion of the rat trachea. Net Chlor influx decreased with increasing duration of exposure to 100% O2 from control levels of 37.0 +/- 2.4 ng.min-1.trachea-1 to 30.0 +/- 1.0 ng.min-1.trachea-1 after 36 h of exposure to 100% O2 and was further depressed after 48 h of exposure to 100% O2 60 23.0 +/- 0.9 ng.min-1.trachea-1. Examination of the O2-exposed tracheas by light microscopy showed normal morphology. In contrast, net Chlor influx was not affected by exposure to 50% O2 for 48 h. In a separate group of rats recovery from the effects of hyperoxia was studied. Within 24 h after removal from the hyperoxic environment, net Chlor influx had returned to control levels. We conclude that high partial pressures of oxygen inhibit net Chlor influx in the rat trachea at a time when tracheal histology is normal. This inhibition is a function of the partial pressure of oxygen and the duration of exposure and it is reversible after removal from the hyperoxic environment.
 ...
PMID:Effects of hyperoxia on transtracheal chloramphenicol influx. 720 97

This study compared the effects of inspiring either a hyperoxic (60% O(2)) or normoxic gas (21% O(2)) while cycling at 70% peak O(2) uptake on 1) the ATP derived from substrate phosphorylation during the initial minute of exercise, as estimated from phosphocreatine degradation and lactate accumulation, and 2) the reliance on carbohydrate utilization and oxidation during steady-state cycling, as estimated from net muscle glycogen use and the activity of pyruvate dehydrogenase (PDH) in the active form (PDH(a)), respectively. We hypothesized that 60% O(2) would decrease substrate phosphorylation at the onset of exercise and that it would not affect steady-state exercise PDH activity, and therefore muscle carbohydrate oxidation would be unaltered. Ten active male subjects cycled for 15 min on two occasions while inspiring 21% or 60% O(2), balance N(2). Blood was obtained throughout and skeletal muscle biopsies were sampled at rest and 1 and 15 min of exercise in each trial. The ATP derived from substrate-level phosphorylation during the initial minute of exercise was unaffected by hyperoxia (21%: 52.2 +/- 11.1; 60%: 54.0 +/- 9.5 mmol ATP/kg dry wt). Net glycogen breakdown during 15 min of cycling was reduced during the 60% O(2) trial vs. 21% O(2) (192.7 +/- 25.3 vs. 138.6 +/- 16.8 mmol glycosyl units/kg dry wt). Hyperoxia had no effect on PDH(a), because it was similar to the 21% O(2) trial at rest and during exercise (21%: 2.20 +/- 0.26; 60%: 2.25 +/- 0.30 mmol.kg wet wt(-1).min(-1)). Blood lactate was lower (6.4 +/- 1.0 vs. 8.9 +/- 1.0 mM) at 15 min of exercise and net muscle lactate accumulation was reduced from 1 to 15 min of exercise in the 60% O(2) trial compared with 21% (8.6 +/- 5.1 vs. 27.3 +/- 5.8 mmol/kg dry wt). We concluded that O(2) availability did not limit oxidative phosphorylation in the initial minute of the normoxic trial, because substrate phosphorylation was unaffected by hyperoxia. Muscle glycogenolysis was reduced by hyperoxia during steady-state exercise, but carbohydrate oxidation (PDH(a)) was unaffected. This closer match between pyruvate production and oxidation during hyperoxia resulted in decreased muscle and blood lactate accumulation. The mechanism responsible for the decreased muscle glycogenolysis during hyperoxia in the present study is not clear.
 ...
PMID:Effects of hyperoxia on skeletal muscle carbohydrate metabolism during transient and steady-state exercise. 1537 50