Therapeutic mechanisms of action for hyperbaric oxygen (HBO2) therapy are based on elevation of both the partial pressure of inspired O2 and of the hydrostatic pressure. This last mechanism contributes to a compression of all gas-filled spaces in the body (Boyle's Law) and is relevant to treat conditions where gas bubbles are present in the body and cause the disease (e.g., intravascular embolism; decompression sickness with intravascular or intra-tissue bubbles). However, the majority of patients treated with HBO2 do not suffer from bubble-induced injuries, but derive clinical improvements from the elevated O2 partial pressures. High O2 partial pressures in various tissues increase the production of reactive O2 species (ROS) and also of reactive nitrogen species (RNS) because of hyperoxia. Most controlled studies have verified that the clinical efficacy from HBO2 derives from modulation of intracellular transduction cascades, leading to synthesis of growth factors and promoting wound healing and ameliorating post-ischemic and post-inflammatory injuries.
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