Optimization of intermittent oxygen/air exposure protocols prolongs the safe use of hyperoxia

A steadily growing body of data indicates that hyperoxia (the use of oxygen at pressures that are higher than its normal atmospheric partial pressure) exerts an extensive profile of physiologic and pharmacologic effects that improve tissue oxygenation, exert anti-inflammatory and anti-bacterial effects, and augment tissue repair mechanisms. Such data establish the rational for the use of normobaric and hyperbaric hyperoxia in a list of clinical conditions characterized by tissue hypoxia, inflammation, infection, and impaired tissue healing. The major limitation confronting the clinical use of hyperoxia is its potential toxicity and the relatively narrow margin of safety that exists between its effective and toxic doses. The most obvious toxic manifestations of oxygen are those exerted on the respiratory and central nervous systems. At pressures higher than 0.6 ATA (atmospheres absolute), (e.g. 60% oxygen at normal atmospheric pressure), and up to 2.8 ATA the most important toxic effect of hyperoxia is a pulmonary inflammatory response that may culminate to a full blown ARDS (Acute Respiratory Distress Syndrome). At pressures higher than 2.8 ATA the most prominent toxic effect of hyperoxia is on the brain, usually manifesting as tonic-clonic grand-mal type convulsions. Currently employed hyperoxic treatment protocols or exposures to oxygen in recreational and military diving are safe because they are restricted to durations that are significantly shorter than the latent period required for development of toxic effects. Another currently employed approach to effective safe use of hyperoxia is... [J Exp Integr Med 2012; 2(4): 283-285]