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The content and information provided within this site is for informational and educational purposes only. Consult a doctor before pursuing any form of therapy, including Hyperbaric Oxygen Therapy. The Information provided within this site is not to be considered Medical Advice. In Full Support of the F.D.A., Hyperbaric Oxygen Therapy is considered Investigational, Experimental, or Off Label.

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What are the Beneficial Mechanisms

Several beneficial mechanisms are associated with intermittent exposure to hyperbaric doses of oxygen. Either alone, or more commonly in combination with other medical and surgical procedures, these mechanisms serve to enhance the healing process of treatable conditions.

  1. HYPEROXYGENATION: provides immediate support to poorly perfused tissue in areas of compromised blood flow. The elevated pressure within the hyperbaric chamber results in a 10-15-fold increase in plasma oxygen concentration. This translates to arterial oxygen values of between 1,500and 2000 mmHg, thereby producing a four-fold increase in the diffusing distance of oxygen from functioning capillaries. While this form of hyper-oxygenation is only a temporary measure, it will often serve to buy time and maintain tissue viability until corrective measures can be implemented or a new blood supply established.
  2. NEOVASCULARIZATION: represents an indirect and delayed response to hyperbaric oxygen exposure. Therapeutic effects include enhanced fibroblast division, neo-formation of collagen, and capillary angiogenesis areas of sluggish neovascularization such as late radiation damaged tissue, refractory osteomyelitis, and chronic ulcerations in soft tissue.
  3. Hyperoxia enhanced ANTIMICROBIAL ACTIVITY has been demonstrated at a number of levels. Hyperbaric oxygen causes toxin inhibition and toxin inactivation in Clostridial perfringens infections (gas gangrene). Hyperoxia enhances phagocytosis and white cell oxidative killing, and has been shown to enhance amino glycocide activity. Recent research has demonstrated a prolonged post-antibiotic effect, when hyperbaric oxygen is combined with tobramycin against Pseudomonas aeroginosa.
  4. DIRECT PRESSURE: utilizes the concept of Boyle's Law to reduce the volume of intravascular or other free gas. For more than a century, this mechanism has formed the basis for hyperbaric oxygen therapy as the standard of care for decompression sickness and cerebral arterial gas embolism. Commonly associated with divers, CAGE is a frequent iatrogenicevent in modern medical practice. It results in significant morbidity and mortality and remains grossly under diagnosed.
  5. Hyperoxia-induced VASOCONSTRICTION is another important mechanism. It occurs without component hypoxia, and is helpful in managing intermediate compartment syndrome and other acute ischemias in injured extremities, and reducing interstitial edema in grafted tissue. Studies in burn wound applications have indicated a significant decrease in fluid resuscitation requirements when hyperbaric oxygen therapy is added to standard burn wound management protocols.
  6. ATTENUATION OF REPERFUSION INJURY: is the most recent mechanism to be discovered. Much of the damage associated with reperfusion is brought about by the inappropriate activation of leukocytes. Following an ischemic interval, the total injury pattern is the result of two components: a direct irreversible injury component from hypoxia, and an indirect injury, which is largely mediated by the inappropriate activation of leukocytes. Hyperbaric oxygen reduces the indirect component of injury by preventing such activation. The net effect is the preservation of marginal tissues that may otherwise be lost to ischemia- reperfusion injury.

Reprinted with permission