HBOT affects the body’s “inflammatory reaction,” and this is key to comprehending the vast number of applications for HBOT. Inflammation is a protective attempt to remove the cause of injury—burns, chemical irritants, frostbite, toxins, infection, physical injury, immune reactions, ionizing radiation, etc.—and to start the healing process. Without this process wounds and infections would not heal and progressive destruction of the tissue would ensue. On the other hand, both acute and chronic inflammation can cause secondary damage in their own right.
Acute inflammation is the initial response of the body to harmful stimuli—usually within a few minutes or hours—and is characterized by pain, redness, immobility, swelling, bruising and heat. Redness and heat are due to increased blood flow to the injured site, swelling is caused by fluid accumulation and pain results from the release of chemicals that stimulate nerve endings—unless the area does not have pain-sensitive nerve endings. This reaction also happens in the brain, heart and other organs when injury occurs.
Acute inflammation involves the movement of plasma and leukocytes (white blood cells), especially granulocytes, from the blood into the tissues. A whole cycle of biochemical processes ensues and propels the inflammatory response involving the local vascular system, the immune system and cells within the injured tissue. Chronic inflammation produces a change in the type of cells predominant at the site. There is simultaneous destruction and healing of the tissue due the inflammatory process.
Acute inflammation is started by cells already present in all tissues: macrophages, dendritic cells, histiocytes, Kupffer cells and mastocytes. At the onset of injury these cells are activated and release inflammatory mediators that result in the clinical signs of inflammation. Vasodilatation and its resulting increased blood flow produces redness and heat. Increased permeability of the blood vessels results in leakage (exudation) of plasma proteins and fluid into the tissue (edema) resulting in swelling. Released mediators such as bradykinin increase pain sensitivity. Other mediator molecules alter the blood vessels to allow the migration of leukocytes, mostly neutrophils, outside the blood vessels (extravasation) into the tissue.
In addition to cell mediators, other biochemical cascade systems are involved. These involve preformed plasma proteins that act together to both start and propagate the inflammatory response. The complement system is activated by bacteria, while the coagulation and fibrinolysis systems are activated by necrosis—burn or trauma. In an acute inflammatory response the inflammatory mediators have short half-lives and are rapidly degraded in the tissue. Inflammation subsides once the stimulus has been removed.
In chronic inflammation the immune cells mistake fatty deposits for intruders and the body then attacks fat similar to bacteria and fungi. Macrophages arrive to clean up and embed into adipose tissue. Then macrophages release inflammatory chemicals, including tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6). The TNFs induce inflammation, white blood cells then try to help by releasing more cytokines, which produces more inflammation. C-Reactive Protein (CRP) is produced at higher levels in obese people. It is a marker for inflammation throughout the body, and increases the risk of heart attacks, strokes, high blood pressure, muscle weakness, etc.
Chronic inflammation may lead to a chronic wound and is characterized by the dominance of macrophages in the injured tissue. While these cells are effective defensive agents their toxins are injurious to the body’s tissues as well as the invading agents. Because of this, chronic inflammation is almost always accompanied by tissue destruction.
The initial low oxygen and low blood flow common to many chronic wounds seems to “freeze” or “stun” cells in an injured area.20
Chronic inflammation results when the mechanisms that turn off the inflammatory response don’t kick in. Cellular destruction continues and chronic inflammation results in amyloidosis. These proteins include C-reactive protein, serum amyloid A, and serum amyloid P, vasopressin; these cause a spectrum of systemic effects: fever, increased blood pressure, decreased sweating, malaise, loss of appetite, and fatigue.