On the pulmonary toxicity of oxygen. 5. Electronic structure and the paramagnetic property of oxygen

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Oxygen toxicity
Lung injury
Hyaline membrane disease
Respiratory distress
Molecular attributes
Electron shell saturation
Redefinition of hypoxia
Rate of lesion formation
Oxygen uptake by the pulmonary circulation is a chemical reaction. The physicochemical attributesof oxygen are critical when studying pulmonary oxygen toxicity. Extent of lung injury depends onthe percentage of oxygen in an oxygen:nitrogen mix in polybaric circumstances (Shanklin, 1969). Further change in extent of lesion follows when other gases are used in the inhalant mix instead of nitrogen (Shanklin and Lester, 1972), with oxygen at 21-100% of the mix. Comparative subatmospheric oxygen levels down to 3% in hydrogen, helium, nitrogen, argon, or sulfurhexafluoride, were run with and without ventilatory distress by the Farber (1937) model, bilateralcervical vagotomy (BCV). This yielded coherent results indicating a need to consider molecular characteristics at the atomic level. Molecular mass and size, gas viscosity, and thermal conductivity yielded no obvious correlates to lung injury. Saturation of the outer electron shells of the diluents fit the empiric data, prospectively an interaction between oxygen and nitrogen from their electronegativity and closely approximate molecular mass, size, and shape. The lesion is essentially eliminated at 7% oxygen in nitrogen. At 3% oxygen, the least lesion is found with N2, H2, and SF6,all gases with incomplete outer electron shells, allowing for transient, possibly polarized, covalent bonding with oxygen as the significant minority component in the mix. Argon and helium do not interfere with oxygen. With 3% oxygen in argon without BCV, the experiments ran so long (>70hours) they were terminated once the point had been made. 3% oxygen in argon after BCV yielded a mean survival more than twice that of BCV in air, indicating a remarkable degree of nitrogen interference with oxygen in the respiratory medium of terrestrial animal life. Argon displayed other advantages for the lung compared to nitrogen. Hydrogen, nitrogen, and oxygen are diatomic molecules, a feature which does relate to the extent of lung injury, but only oxygen is paramagnetic. Magnetic effects on lesion formation were tested: [1] with ventilatory distress induced in newbornrabbits, and [2] in young adult female white mice exposed to 100% oxygen without addedmechanical distress. A noninvasive model for ventilatory distress, thoracic restraint (TR), withlonger mean survivals of 40-50 hours, was employed rather than the Farber model. Parallel runs with TR, one subset receiving 100% oxygen in a plastic chamber resting on six strong ring magnetswith measured fields up to +1200 gauss, the other plain 100% oxygen, were performed. Bothsubsets developed moderate metabolic acidosis with average weight losses circa 25%, but over different time courses, 82.89 ± 4.91 hours in magnetized oxygen, 55.4 per cent longer than the 53.34 ± 9.82 hours in plain oxygen ( p <0.001). The longer survival in magnetized oxygen meant extensive lung injury (99.57 ± 0.42% pleural surface, versus 83.86 ± 14.03%), but the rate of lesionformation was 30.89 per cent faster in plain oxygen (1.5722% per hour) than in magnetized oxygen(1.2012% per hour), a difference significant at p <0.001. The effect of oxygen without mechanical ventilatory distress was examined in female adult whitemice exposed to oxygen or magnetized oxygen. Similar survivals and weight losses were achieved. The rate of lung lesion formation was different, 1.2617% per hour in plain oxygen, 46.13 per centfaster than 0.8634% per hour in magnetized oxygen. A variable magnetic field, with animals moving and breathing in chambers flooded with oxygen, has both systemic and pulmonary effectswhich alter the rate of lesion formation due to oxygen toxicity. Paramagnetic oxygen in a magneticfield influences the effect of oxygen toxicity on the lung but at these strengths of field it does notovercome significant mechanical disturbance.
Author Posting. © The Author(s), 2012. This is the author's version of the work. It is posted here by permission of Elsevier B.V. for personal use, not for redistribution. The definitive version was published in Experimental and Molecular Pathology 93 (2012): 365-377, doi:10.1016/j.yexmp.2012.08.007.
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