The Toxicity of Oxygen

Oxygen, the lung and the diver: friends and foes?

“…Over time it became clear that the pathological pathway of POT in animals had a biphasic development, i.e. an acute phase, followed by a chronic phase if oxygen breathing was continued [10][11][12][13]. During the acute phase, exudation appears to be a key feature, which expresses itself as interstitial and alveolar oedema.…”

“…Susceptibility to POT varies widely among species but is also dependent on age, strain and individual susceptibility [10,11,21]. Human lungs exposed to high concentrations of hyperoxia show a sequence of pathological changes similar to those seen in primates [15].…”

“…The rate at which POT develops is directly related to the inspired PO 2 [10,21]. Tracheobroncholitis develops after a latent period of 4-22 h when breathing oxygen with a PO 2 of 95 kPa (713 mmHg), but may occur as early as 3 h while breathing oxygen at 300 kPa (2250 mmHg) [21,24].…”

“…After the exudative reaction subsides, the proliferative phase marks its starts with the proliferation of interstitial fibres and alveolar type 2 cells [25]. In the late proliferative phase interlobular septal oedema, alveolar hyperplasia and fibroblastic proliferation with early fibrosis can be found [10,11]. Oedema and fibrosis are late and end-stage processes in human POT [23].…”

Effects of oxygen exposure on in vitro function of pulmonary alveolar macrophages.

“…No impairment of in vitro bactericidal activity against either S. aureus 502A or Ps. aeruginosa could be demonstrated in PAMs from normal rabbits exposed to 02 for 48 h. These results indicate that the in vitro phagocytic and bactericidal capacity of the rabbit PAM is relatively resistant to the INTRODUCTION The critically ill patient requiring mechanical ventilatory support with high concentrations of oxygen is at significant risk for developing pulmonary oxygen toxicity (1). A common clinical impression is that such patients are also more susceptible to pulmonary bacterial infections (2).…”