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

To study extension of O2 tolerance by interruption of hyperoxic exposure, as compared to previous studies of continuous oxygen exposure, five healthy volunteers were exposed to oxygen at 2 ATA on an intermittent schedule of 20 min breathing O2, alternating with 5 min on a normoxic N2-O2 mixture. The cycle was repeated until symptoms or signs of O2 toxicity caused cessation of the experiment. Tracheal irritation and burning on inspiration occurred after 6-9 "oxygen hours" of exposure and progressed to severe tracheobronchial burning sensation, chest pain, and dyspnea after 11-15 h of O2. Average duration of exposure was 13.7 O2 h, inducing a mean vital capacity decrease of 10.3%. The decrease began soon after onset of symptoms. With intermittent O2 administration, nearly a doubling of the average duration of actual oxygen breathing was required to induce marked vital capacity change (greater than 10%) as compared to the previous studies of continuous O2 exposure. The increased duration of tolerable O2 exposure in man resembles the extension of O2 tolerance known to occur in animals exposed to intermittent hyperoxia.
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PMID:Extension of pulmonary O2 tolerance in man at 2 ATA by intermittent O2 exposure. 86 21

Supplemental oxygen is often administered to induce hyperoxia in nonhypoxic patients for indications such as chest pain, despite lack of evidence of clinical benefit. Induced hyperoxia is potentially toxic, since it may increase oxidative stress and peroxidative damage to deoxyribonucleic acid, lipids and proteins. The aim of this study was to establish whether supplemental oxygen induces oxidative stress in nonhypoxic subjects. Breath markers of oxidative stress were measured in 31 healthy subjects before and after breathing 28% oxygen at 2.0 L x min(-1) via nasal prongs for 30 min while resting. The criterion standard of oxidative stress was the breath methylated alkane contour (BMAC), a three-dimensional plot of the alveolar gradients of C4-C20 alkanes and monomethylated alkanes produced by lipid peroxidation. Volatile organic compounds (VOCs) in breath were assayed by gas chromatography and mass spectroscopy, and the BMACs before and after oxygenation were compared. Following oxygenation, there was a significant increase in mean volume under the curve of the BMAC and in alveolar gradients of three VOCs: 3-methyltridecane, 3-methylundecane and 5-methylnonane. Breath markers of oxidative stress were significantly increased in normal volunteers breathing supplemental oxygen for 30 min.
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PMID:Effect of oxygen on breath markers of oxidative stress. 1257 Jan 8