Within just a short time after the discovery of oxygen 200 years ago, Joseph Priestley, one of its codiscoverers, was already cautioning that oxygen "might burn the candle of life too quickly, and too soon exhaust the animal powers within."1 Priestley's prescient speculations about the toxic nature of excess O2. have been confirmed by a host of succeeding investigators.
Today, most clinicians are well aware of the toxic consequences to the lung of prolonged exposure to high tensions of O2, yet physicians involved in intensive care are frequently confronted by situations in which prolonged hyperoxic therapy is a necessary part of the management of neonatal and adult patients with severe respiratory distress. Unfortunately, no pharmacological agent is available to help circumvent the development of pulmonary toxicity associated with prolonged high oxygen therapy. The spectrum of O2-induced lung injury, including pulmonary edema, atelectasis, consolidation, congestion, hemorrhage,