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?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.

Cardiac chest pain is accompanied by oxidative stress, which generates alkanes and other volatile organic compounds (VOCs). These VOCs are excreted in the breath and could potentially provide a rational diagnostic marker of disease. The breath methylated alkane contour (BMAC), a 3-dimensional surface plot of C4-C20 alkanes and monomethylated alkanes, provides a comprehensive set of markers of oxidative stress. In this pilot study, we compared BMACs in patients with unstable angina pectoris and in healthy volunteers. Breath VOCs were analyzed in 30 patients with unstable angina confirmed by coronary angiography and in 38 age-matched healthy volunteers with no known history of heart disease (mean age +/- SD, 62.7 +/- 12.3 years and 62.5 +/- 10.0, not significant). BMACs in both groups were compared to identify the combination of VOCs that provided the best discrimination between the 2 groups. Forward stepwise entry discriminant analysis selected 8 VOCs to construct a predictive model that correctly classified unstable angina patients with sensitivity of 90% (27 of 30) and specificity of 73.7% (28 of 38). On cross-validation, sensitivity was 83.3% (25 of 30) and specificity was 71.1% (27 of 38). We conclude that the breath test distinguished between patients with unstable angina and healthy control subjects.

The effect of crystalloid volume loading on serum colloid osmotic pressure, arterial oxygen (Po2), alveolar-arterial oxygen gradient (A-aDo2), and cerebral lateral ventricle dimensions was prospectively studied in 18 patients with diabetic ketoacidosis. Serial measurements showed concomitant decreases in colloid osmotic pressure, hematocrit, arterial Po2 (p less than 0.001), and significant increases in A-aDo2 (p less than 0.001) during treatment. Serial echoencephalograms were taken of 11 of the 18 patients; each patient served as his or her own control. Nine of these 11 patients showed significant decreases in lateral ventricle width during treatment; seven patients showed the echoencephalographic "hash" marks characteristic of cerebral edema. Follow up studies showed resolution of these abnormalities. Volume loading with large amounts of crystalloid solution seems to produce an acute hypooncotic state that may cause the development of both subclinical pulmonary and cerebral edema.

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