• A Møllerløkken, S E Gaustad, M B Havnes, C R Gutvik, A Hjelde, U Wisløff, and A O Brubakk.
• Baromedical and Environmental Physiology Group, Department of Circulation and Medical Imaging, Norwegian University of Science and Technology, Medisinsk teknisk forskningssenter, Olav Kyrres gt 9, 7489, Trondheim, Norway. andreas.mollerlokken@ntnu.no
• Eur. J. Appl. Physiol. 2012 Feb 1; 112 (2): 401-9.

AbstractA key process in the pathophysiological steps leading to decompression sickness (DCS) is the formation of inert gas bubbles. The adverse effects of decompression are still not fully understood, but it seems reasonable to suggest that the formation of venous gas emboli (VGE) and their effects on the endothelium may be the central mechanism leading to central nervous system (CNS) damage. Hence, VGE might also have impact on the long-term health effects of diving. In the present review, we highlight the findings from our laboratory related to the hypothesis that VGE formation is the main mechanism behind serious decompression injuries. In recent studies, we have determined the impact of VGE on endothelial function in both laboratory animals and in humans. We observed that the damage to the endothelium due to VGE was dose dependent, and that the amount of VGE can be affected both by aerobic exercise and exogenous nitric oxide (NO) intervention prior to a dive. We observed that NO reduced VGE during decompression, and pharmacological blocking of NO production increased VGE formation following a dive. The importance of micro-nuclei for the formation of VGE and how it can be possible to manipulate the formation of VGE are discussed together with the effects of VGE on the organism. In the last part of the review we introduce our thoughts for the future, and how the enigma of DCS should be approached.

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