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Oxygen therapy pulmonary toxicity

Interruption of oxygen administration decreases the toxic effects on the pulmonary and cerebral nervous system, especially if the periods of exposure to oxygen are of short duration (K5, P9). However, there is evidence that even routine oxygen therapy may give rise to pulmonary alterations (P18). [Pg.95]

Ohlssen, W. T. L., A study on oxygen toxicity at atmospheric pressure with special references to the pathogenesis of pulmonary damage and clinical oxygen therapy. Acia Med. Scand. Suppl. 190, 1-93 (1947). [Pg.134]

Mitomycin is an alkylating antibiotic that produces pulmonary fibrosis at a frequency of 3% to 12%. The mechanism is unknown, but oxygen and radiation therapy appear to enhance the development of toxicity. The clinical presentation and symptoms are the same as for bleomycin. The mortality rate is about 50%. Early withdrawal of the drug and administration of corticosteroids appear to improve the outcome significantly. [Pg.586]

There is no recognized prophylactic therapy for human PFIB exposure. Animal studies suggest that increasing pulmonary concentrations of oxygen free-radical scavengers containing thiol groups may be of value N-acetyl cysteine has been found effective.65,66 No postexposure medical or chemical therapy that effectively impedes or reverses the effects of this toxic inhalational injury is known. [Pg.266]


See other pages where Oxygen therapy pulmonary toxicity is mentioned: [Pg.250]    [Pg.242]    [Pg.569]    [Pg.585]    [Pg.585]    [Pg.586]    [Pg.587]    [Pg.813]    [Pg.139]    [Pg.304]    [Pg.1382]    [Pg.1641]    [Pg.79]    [Pg.492]    [Pg.361]    [Pg.366]    [Pg.467]    [Pg.446]    [Pg.635]    [Pg.818]   
See also in sourсe #XX -- [ Pg.582 , Pg.583 , Pg.584 , Pg.584 ]




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