Hyperbaric oxygen (HBO2) therapy is defined as breathing 100% oxygen (O2) at a pressure greater than 1.4 atmospheres absolute (ATA) (1). HBO2 is currently accepted as a clinical adjunctive therapy for the following indications: wound healing, carbon monoxide (CO) poisoning, crush injury, clostridial myositis and myonecrosis, decompression sickness, osteomyelitis (refractory), skin grafts and flaps, and air or gas embolism (1–3). HBO2 therapy is administered in either a monoplace hyperbaric chamber (where the chamber is compressed with 100% oxygen) or in a multiplace hyperbaric chamber (where the chamber is compressed with air and the patient breathes 100% oxygen via a tight-fitting mask or hood) (Figure 53.1).Many benefits of HBO2 therapy are gained through its effects on the endothelium, including improvements in microvascular flow, induction of proangiogenic factors, inhibition of inducible intercellular adhesion molecule (ICAM)–1 expression, and regulation of endothelial derived nitric oxide (NO) production. The ubiquitous nature of the endothelium provides a gateway for many of the HBO2 protective mechanisms to be effective at a number of injury sites. This chapter reviews the effects of HBO2 therapy on disease states that are most dependent on endothelial responses: wound healing and ischemia–reperfusion (I/R) injury.

HISTORY OF HYPERBARIC OXYGEN THERAPY

HBO2 therapy was born from the concept that individuals exposed to increased ambient air pressure would have improvement in many different disease states (4). Although there was no scientific basis for this concept, it was put into practice as early as 1662 by a British clergyman, Henshaw (5). Compressed-air therapy enjoyed a nonscientifically founded popularity during the 19th century in a manner similar to mineral water spas (6).