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WITH the increasing use of oxygen at greater than atmospheric partial pressure for treatment of patients and for clinical research, it is inevitable that oxygen intoxication is also being induced. To provide for a rational extension of oxygen therapy, the tolerance to hyperoxia of individual cell types and organ systems, normal and diseased, must be established. Although oxygen appears able to damage or destroy any tissue, the implications of oxygen toxicity vary with the structure affected. The response of the normal lung to hyperoxia has been extensively studied, primarily because it is the first organ to come in contact with . . .
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Nichols et al. (1969) studied this question.
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