Decompression sickness (DCS) is caused by gas bubbles that form in the body during and after decompression. The current thought is that gas bubbles originate on the venous side and pass to the arterial side either through intra-cardiac (PFO) or intra-pulmonary shunt (arteriovenous anastomoses). A group of scientists proposed recently a third mechanism: the evolution of bubbles in the distal arteries, independent of venous gas bubbles.1 They presented their work at the European Underwater and Baromedical Society’s (EUBS) 2017 conference.
They base their theoretical work on previous experimental studies which identified so called “active hydrophobic spots” (AHS) on inner surface of blood vessels.3 Atomic force microscopy showed that on these spots tiny formations of gas bubbles, between 5 and 30 nm in diameter, were forming spontaneously. These formations are thousands of times smaller than venous gas bubbles, and if released into circulation they would probably be crushed immediately. However, in some specific conditions they could grow and reach the size of viable gas bubbles.
This may happen in two stages.
The first stage of this condition occurs during decompression, when nano bubbles increase to the size of micro bubbles and are released into circulation. In the following second stage, bubbles grow due to simple diffusion of gas from the blood. Favorable conditions for this may occur in small arteries with thin walls, through which inert gas from surrounding tissues may diffuse into the bloodstream. The smaller the artery, the more gas diffuses into it. These smaller arteries also have significantly slower blood flow, which enables an increase in the partial pressure of the inert gases. In normal conditions this contributes to a one-percent increase of inert gas partial pressure in small cerebral arteries which does not cause much trouble. However, if the circulation slows down another 10 percent, the partial pressure increases by 44 percent, and this increase can contribute to a significant growth of microbubbles, occlusion of terminal arteries, and damage of the tissues manifesting as decompression sickness.
In the view of the authors, this proposed mechanism could explain some of the characteristics of DCS, like predominance of spinal cord DCS, effects of repetitive diving, variability of individual sensitivity to DCS, effects of aging and acclimation.
This is an interesting approach and we can expect significant results in this vein of research in the future. For now, those interested in decompression modelling should read the original papers, which are available online for free.
References
- Arieli R, Marmur A. A biophysical vascular bubble model for devising decompression procedures. Physiol Rep, 5 (6), 2017, e13191, doi: 10.14814/phy2.13191
- Arieli R. A new model of arterial decompression bubble development and spinal DCI. Abstract and Conference Book, EUBS 43 Annual Scientific Meeting, Ravenna (Italy), 12-18 September 2017, p 30.
- Arieli R. Nanobubbles Form at Active Hydrophobic Spots on the Luminal Aspect of Blood Vessels: Consequences for Decompression Illness in Diving and Possible Implications for Autoimmune Disease—An Overview. Front. Physiol. 8:591. doi: 10.3389/fphys.2017.00591.