Venous gas embolism as a predictive tool for improving CNS decompression safety

A 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

Release of VCAM-1 associated endothelial microparticles following simulated SCUBA dives

Microparticles (MP) are shed into the circulation from endothelium following activation or apoptosis. Vascular cell adhesion molecule-1 (VCAM-1) is expressed on endothelial cells following activation and here we report quantification of VCAM-1 positive microparticles (VCAM + MP) following simulated SCUBA dives, breathing either air or oxygen. VCAM + MP were quantified pre-dive (09:00 and 13:00) and post-dive (+1, +3 and +15 h) on both air and oxygen dives and compared with control samples taken from the same subjects. VCAM + MP followed a similar trend in all experiments, however both dives caused a change in endothelial state, as measured by VCAM + MP. A significant increase in VCAM + MP was observed 1 h post-air dive relative to the control (p = 0.013), which was not observed after the oxygen dive (p = 0.095). Oxidative stress (TBARS) was correlated with VCAM + MP. Data presented highlights the potential of MP as a biological marker of both endothelial state and decompression illness