Diving and the blood vessels
Guerrero, F.; Lambrechts, K.; Mazur, A.; Wang, Q.; Dujic, Z (2017). Diving and the blood vessels, in: Balestra, C. et al. The science of diving. Things your instructor never told you. pp. [116-136] In: Balestra, C.; Germonpré, P. (2017). The science of diving. Things your instructor never told you. Lambert Academic Publishing/Éditions Acrodacrolivres: Villers-la-Ville. ISBN 978-2-512007-36-4. [262] pp., more |
| Authors | | Top | - Guerrero, F.
- Lambrechts, K.
- Mazur, A.
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| Abstract | The vascular endothelium is a dynamic organ with important functions for the regulation of vascular activity and plays a key role in homeostasis control. Increased endothelial permeability is commonly involved in decompression sickness (DCS), it is the result of contact loss among microvascular endothelial cells and the weakening of their adhesion to the basement membrane. The impact of diving on the microvascular endothelium has been shown recently by laser Doppler flowmetry and iontophoresis. Flow Mediated Dilation (FMD) measurements also confirm this endothelial dysfunction and an impairment of endothelium-dependent vasoreactivity. This dysfunction may be due to an impairment of vascular smooth muscle (VSM), as has been confirmed by a decrease in VSM sensitivity to nitric oxide (NO). Successive dives have a cumulative short term but not long term effect on vascular function. There is also evidence that this impairment of microcirculatory endothelial function after diving might be preventable or restorable. The impairment is not only due to the presence of bubbles: diving-induced alterations in endothelial and cardiovascular function have also been found in the absence of vascular gas emboli (VGE). Through further investigation was found that oxidative stress was involved in diving-induced FMD changes, confirming that bubble formation is not the only factor involved. The main molecule involved in oxidative stress processes is the Superoxide Anion, which can inactivate NO. Bubble formation and/or DCS are modulated by the bioavailability of endothelium-derived NO. However, it has not been found that impairment of endothelium-derived NO is involved in divinginduced FMD changes. Available data now suggest that vascular dysfunction may result from neutrophil activation generated through platelet-derived microparticles (MPs) during diving and this might be a link in the chain involving oxidative stress, circulating MPs and activation of neutrophils from the initiation of DCS. However, how bubble formation and oxidative stress adjust the vascular and endothelium dysfunctions as well as the impairment of vascular smooth muscle during the development of DCS remains to be studied further. |
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