Both in vivo as well as in vitro studies have demonstrated the following effects of HBOT. When used with 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 perfuse 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 1,500 and 2000 mmHg, thereby producing a four-fold increase in the diffusing distance of oxygen from functioning capillaries to the wound.
2. NEOVASCULARIZATION represents an indirect and delayed response to hyperbaric oxygen exposure. Therapeutic effects include enhanced fibroblast division, neoformation of collagen, and capillary angiogenesis in 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 aminoglycocide 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.
   
   
5. HYPEROXIA-INDUCED VASOCONSTRICTION reduces edema and therefore the distance between the oxygen in the capillaries and the wound itself. It occurs without concomitant hypoxia as the blood that flows thru the vasoconstricted vessels are highly oxygen enriched to begin with. This mechanism is helpful in managing 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.

Edema increases the distance oxygen must diffuse from capillary to the cell. Diffusion of oxygen from the capillary through tissue fluids to the cell decreases by approximately a three-fold factor as distance is increase.
BEFORE HBOT
AFTER HBOT


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.