Mechanisms of Action for Hyperbaric oxygen therapy (HBOT) and wound healing
May 18, 2020
Hyperbaric Oxygen Therapy, or HBOT, is the use of oxygen inside a chamber where the pressure is increased to greater than 1 atmosphere absolute (1ATA) (1).
HBOT has two primary mechanisms of action - Hyperoxygenation and a decrease in bubble size.
- Hyperoxygenation is an application of Henry's law and results from an increase in dissolved oxygen in plasma as a result of increased partial pressure of arterial oxygen.
- Decrease in bubble size is an application of Boyle's law according to which the volume of a bubble decreases directly in proportion to increasing pressure (it is the primary mechanism at work in management of decompression sickness and arterial gas embolism) (2).
Secondary mechanisms of action include-
- Vasoconstriction
- Angiogenesis (new blood vessel formation)
- Fibroblast proliferation (provides the structural framework for our tissues and is critical in wound healing)
- Leukocyte oxidative killing (immune system activation)
- Toxin inhibition and antibiotic synergy (reducing toxins and increasing antibiotic effect) (2).
Hyperoxia in normal tissues causes vasoconstriction which reduces post-traumatic tissue oedema (contributing to treatment of crush injuries, compartment syndromes and burns). This vasoconstriction, however, does not cause hypoxia as this is more than compensated by increased plasma oxygen content and microvascular flow. In other words, you're still getting oxygen to your tissue even if the red blood cells can't squeeze through, as compared to the much smaller oxygen molecules (2).
This is important in our office when considering concussion and brain injuries as we can potentially reduce swelling and further damage while promoting neuroplasticity to restore normal brain activity and reduce potential for long-term symptoms.
Hypoxia is a vital stimulant for angiogenesis, but development of adequate capillary network requires adequate amounts of tissue oxygen concentration. HBOT increaseas the oxygen gradient between the center and periphery of the wound, thus creating a strong angiogenic stimulus. This along with fibroblastic proliferation leads to increased neovascularisation (2).
References
(1) Sahni T, Hukku S, Jain M, Prasad A, Prasad R, Singh K. Recent advances in hyperbaric oxygen therapy. Medicine update. Assoc Physicians India. 2004;14:632–9. [Google Scholar]
(2) Neubauer RA, Maxfield WS. The polemics of hyperbaric medicine. J P and S. 2005;10:15–7.[Google Scholar]