The uses of high concentrations of therapeutic oxygen have expanded in recent decades. This situation came about both from the introduction of ventilation by intubation in the Intensive Care setting and with the use of hyperbaric oxygen for the treatment of anaerobic infections. Furthermore, high concentrations of oxygen have been used in deep sea diving and in aviation and space exploration. With potential side-effects of exposure to high concentrations of oxygen it has become increasingly important to understand better the parameters of exposure that produce toxicity, the mechanisms by which it occurs and the potential protective devices against its tissue-damaging effects. It is the purpose of this review to address these considerations. The reader is also referred to other reviews (Clark and Lambertsen, 1971; Mustafa and Tierney, 1978; Deneke and Fanburg, 1980a; Fisher, 1980; Frank and Massaro, 1980) where certain aspects of the subject may be covered in more detail.

Damage to tissues by oxygen seems to be related more to the partial pressure of oxygen than to its percent concentration. Hence, a high concentration of oxygen may be less damaging at high altitude where the atmospheric pressure is reduced than it is for the same concentration at normobaric pressure. The primary target of injury for normobaric hyperoxia is the lung, probably at least in part because lung cells are exposed to higher partial pressures of oxygen than are other cells of the body. With hyperbaric hyperoxia, the rapid onset of convulsions indicates that the central nervous system shows the earliest signs of toxicity. Hence, with higher partial pressures of oxygen than can be achieved under normobaric conditions, tissues of the central nervous system seem to be" more sensitive" than do cells of the lung. It is likely that certain