How Hyperbaric Oxygen Therapy Works: The Science Behind Pressurized Oxygen

Under normal conditions, your blood carries oxygen almost entirely via hemoglobin. Red blood cells pick it up in the lungs and deliver it to tissue. That system works well until tissue oxygen demand exceeds supply — in infected wounds, damaged bone, stroke-affected brain tissue, or ischemic areas where circulation is compromised.

HBOT bypasses that bottleneck.

Henry’s Law and Plasma Oxygen

Henry’s Law describes a straightforward physical principle: the amount of gas dissolved in a liquid increases in proportion to the partial pressure of that gas above the liquid. Water under a higher oxygen partial pressure dissolves more oxygen.

Your blood plasma behaves the same way. At sea level breathing room air (21% oxygen, 1 ATA), very little oxygen dissolves directly into plasma. At 2.4 ATA breathing 100% oxygen, the partial pressure of oxygen increases approximately 20-fold compared to normal. Oxygen dissolves into plasma in quantities that become clinically meaningful.

That plasma-dissolved oxygen can diffuse into tissue where hemoglobin-carrying red blood cells can’t reach — blocked vessels, capillaries narrowed by diabetes or radiation damage, bone with compromised circulation. The oxygen gets there through simple diffusion, driven by the concentration gradient.

Angiogenesis: Why Wound Protocols Need 20-40 Sessions

A single HBOT session produces a temporary surge in plasma oxygen. It helps, but it doesn’t rebuild blood supply. Repeated sessions do something more durable.

Each session of high oxygen followed by return to normal creates what researchers call a hyperoxic-hypoxic paradox — cycles of oxygen surplus and relative deficit that trigger the body’s repair mechanisms. One of those mechanisms is upregulation of VEGF, vascular endothelial growth factor, the signaling protein that stimulates new blood vessel formation.

This is why chronic wound protocols use 20-40 sessions. Angiogenesis takes time. New vessels have to form, organize, and connect to existing circulation. A 10-session wellness package won’t move this needle.

Stem Cell Mobilization

Thom et al. (2006) found that HBOT doubles the number of circulating CD34+ stem cells — bone marrow-derived progenitor cells that contribute to tissue repair and new blood vessel formation. The mechanism involves nitric oxide synthesis in bone marrow. (PMID: 16361500)

This is one of the more interesting discoveries in HBOT research over the past 20 years. It suggests HBOT’s repair effects aren’t limited to direct oxygen delivery — the treatment also activates the body’s own repair cell population. The clinical relevance for different conditions is still being studied.

Bactericidal Effects

Two distinct mechanisms make HBOT useful against certain infections.

First, high tissue oxygen is directly toxic to anaerobic bacteria — organisms that evolved without oxygen exposure and can’t tolerate it. Gas gangrene (Clostridium perfringens) and some necrotizing soft tissue infections involve anaerobic organisms. HBOT kills them or stops their growth.

Second, neutrophils — the white blood cells that destroy bacteria through oxidative burst — require oxygen to function at full capacity. In hypoxic tissue, neutrophils are present but operating at reduced effectiveness. HBOT restores their killing capacity. This matters in infected diabetic wounds where the wound bed is chronically hypoxic.

Anti-Inflammatory Effects in Acute Injury

In acute injury situations, HBOT reduces pro-inflammatory signaling. It decreases beta-2 integrin expression on neutrophils, which reduces inappropriate neutrophil adhesion and the inflammatory cascade that causes reperfusion injury.

This is why HBOT for decompression sickness isn’t just about bubble size. Bubbles trigger inflammation that causes ongoing tissue damage even after the gas itself is resolved. HBOT addresses both the mechanical bubble problem and the inflammatory response.

Neurological Effects: Blood Flow and Neuroplasticity

For brain conditions — TBI, post-stroke neurological deficits, PTSD in some research — the proposed mechanisms involve cerebral blood flow and neuroplasticity.

In chronically hypoxic or injured brain regions, neurons can be dormant rather than dead. They’ve reduced metabolic activity to survive with limited oxygen supply. Some researchers call these areas “idling neurons.” HBOT’s oxygen increase can restore activity to these cells and, with repeated sessions, promote synaptic reorganization.

Imaging studies have shown increased regional cerebral blood flow following HBOT protocols. The Efrati lab and others have used SPECT and MRI to document changes in brain perfusion patterns before and after treatment. Whether those changes correlate with functional improvement varies by patient and condition.

Pressure as a Mechanism: Decompression Sickness

For DCS and arterial gas embolism, the pressure itself — not just the oxygen — is part of the treatment. Boyle’s Law states that gas volume decreases as pressure increases. Recompressing a patient with nitrogen bubbles in tissue physically reduces bubble size, restoring circulation to blocked vessels and reducing mechanical tissue damage.

Combined with 100% oxygen breathing (which washes out nitrogen faster and prevents additional bubble formation), this is why recompression is the treatment for DCS rather than just breathing oxygen at normal pressure.

FAQ

Does more pressure mean better results? Not necessarily. Most wound protocols use 2.4 ATA. Going higher increases oxygen toxicity risk without demonstrated additional benefit for most indications. The optimal pressure varies by condition — treatment tables are based on decades of research, not guesswork.

Why does HBOT help conditions that seem very different from each other? Because hypoxia is a common pathway in many conditions. Wounds don’t heal because cells can’t get enough oxygen. Bone infections persist partly because neutrophils can’t kill bacteria in low-oxygen tissue. Some brain injuries leave neurons dormant in low-oxygen zones. Delivering more oxygen to struggling tissue helps across these different contexts, but through different specific mechanisms in each case.

Does HBOT work differently in the brain than in wounds? Yes. In wounds, angiogenesis and bactericidal effects are the primary mechanisms. In brain conditions, researchers focus on cerebral blood flow, neuroplasticity, and stem cell recruitment. The fundamental Henry’s Law physics is the same, but the therapeutic effect builds on different biology depending on the target tissue.

Medical Disclaimer: This page describes proposed mechanisms of action based on published research. It is not medical advice. The specific mechanisms relevant to your condition should be discussed with a qualified hyperbaric medicine physician.

Related guides: What Is Hyperbaric Oxygen Therapy? | How HBOT Helps Diabetic Wounds | Decompression Sickness and HBOT