Oxidative stress is fundamental to hyperbaric oxygen therapy

THERAPEUTIC MECHANISMS OF action for hyperbaric oxygen(HBO2) are based on elevation of both the partial pressure ofoxygen and hydrostatic pressure. Elevating the hydrostaticpressure increases partial pressure of gases and causes a reductionin the volume of gas-filled spaces according to Boyle’slaw. These actions have direct relevance to treating pathologicalconditions in which gas bubbles are present in the body,such as arterial gas embolism and decompression sickness. Themajority of patients who undergo HBO2 therapy are not treatedfor bubble-induced injuries; hence therapeutic mechanisms arerelated to an elevated O2 partial pressure. A summary of thesemechanisms is shown in Fig. 1.It is well accepted that reactive oxygen species (ROS)mediate O2 toxicity, which for HBO2 encompasses pulmonaryinjuries, central nervous system effects manifested by grandmal seizures, and ocular effects such as reversible myopia (29).ROS and reactive nitrogen species (RNS) also serve as signalingmolecules in transduction cascades, or pathways, for avariety of growth factors, cytokines, and hormones (4, 25, 82,123). As such, reactive species can generate either “positive”or “negative” effects depending on their concentration andintracellular localization. Although more is still to be learnedabout the role ROS and RNS play in therapeutic responses ofHBO2, this review will take stock of how far the field hasprogressed. The review will be organized around major categoriesof problems or processes where controlled clinical trialshave demonstrated clinical efficacy for HBO2.