Was the appearance of surfactants in air breathing vertebrates ultimately the cause of decompression sickness and autoimmune disease?

All air breathing vertebrates are endowed with pulmonary surfactants, surface-active lipoprotein complexes formed by type II alveolar cells. Surfactants are deposited in clearly defined areas on the luminal aspect of blood vessels, producing hydrophobic spots. Gas nanobubbles measuring 5-100nm form spontaneously on the smooth hydrophobic spot from dissolved gas. Bubbles nucleate and grow at these spots after decompression from high pressure. Proteins with hydrophobic regions circulating in the blood will adhere to the gas phase-plasma interface. Deformation of their secondary and tertiary configuration will present them as foreign molecules or autoantigens. Components of the intact protein which are also present in a deformed protein may be recognized as foreign too. This process is proposed as the trigger for autoimmune diseases. The presence of autoimmune disease in air breathing vertebrates, increased autoimmunity and the elevated risk of decompression sickness with age, as well as variable sensitivity to both diseases, can be matched with the appearance of surfactant spots. Eliminating these spots may provide protection against both diseases.

Partial pressure of nitrogen in breathing mixtures and risk of altitude decompression sickness.

BACKGROUND: Many aircraft oxygen systems do not deliver 100% O2. Inert gases can be present at various levels. The purpose of this study was to determine the effect of these inert gas levels on decompression sickness (DCS). METHODS: Subjects were exposed for 4 h to 5486 m (18,000 ft) with zero prebreathe, using either mild (Test A) or strenuous exercise (Test B), and breathing 60%N2/40%O2. Test C used a breathing mixture of 40%N2/60%O2 at 6858 m (22,500 ft) with zero prebreathe and mild exercise. Test D investigated a breathing mixture of 2.8%N2/4.2%argon/93%O2 with 4 h exposures to 7620 m (25,000 ft), mild exercise, and 90 min of preoxygenation. The controls were from previous studies using similar conditions and 100% O2. RESULTS: The DCS risk for Tests A and B and the Control for B was 7%; the Control for Test A was 0% (n.s.). Breathing the 40%N2/60%O2 mixture (Test C) resulted in 43% DCS compared with 53% DCS with 100% O2 (n.s.). When the 2.8%N2/4.2%argon/93%O2 mixture was used, the results showed 25% DCS compared with 31% DCS with 100% O2 (n.s.). CONCLUSIONS: The increased nitrogen and argon levels in the breathing gas while at altitudes of 5486 m to 7620 m did not increase DCS risk. These results support the concept of using the partial pressure gradient of inert gases instead of the percentage of N2 or argon in a breathing gas mixture to determine the risk of DCS during altitude exposure.

Delayed onset pulmonary barotrauma or decompression sickness? A case report of decompression-related disorder.

A-24-yr-old male professional diver began to complain of substernal pain 3 h after a controlled ascent from a dive of less than 40 ft of sea water (fsw). The diving master who supervised his dive and the physicians who examined him on presentation suspected pulmonary barotrauma rather than decompression sickness (DCS) because he had only descended to a depth of 32 fsw. Hyperbaric oxygen therapy (HBO) by U.S. Navy treatment Table VI was implemented because of his progressively worsening pain. HBO was apparently effective and a relapse was not seen. The author cannot label his condition based on the conventional classification categories, such as decompression sickness (DCS), barotrauma or even decompression illness. This case report is offered as a topic for consideration in the controversy over decompression-related disorders.