The EUBS annual scientific conference in Geneva, September 2016 presented several papers about endothelial dysfunction in diving. The endothelium is the layer of cells on the inner surface of blood vessels. It is very active in regulation of local blood flow, self-repair, prevention of blood coagulation and inflammatory response to various insults. An important mediator in activities of endothelium is nitric oxide (NO) which regulates also the constriction and dilatation of vessels. This has been found affected by diving due to hyperoxia which limits the availability of NO and thus reduces ability of vessels to dilate following temporary occlusion (flow-mediated dilatation; FMD). Injury of endothelium, which can be caused by bubbles, results in increased quantities of released cell fragments called endothelial micro particles (EMPs). The study of possible roll of FMD and EMPs in diving is confounded by variety of stressors that contribute to their changes, like exercise and thermal stress. However, the potential to explain mechanisms of decompression illness keep these topics in the focus of scientists.
The group from the Second Military Medical University, Shanghai,(1) studied effects of bubbles in isolated endothelial cells (in vitro) and in vivo. They have shown that contact with bubbles increases the release of EMPs. They collected the EMPs and brought it in contact with normal endothelial cells without presence of bubbles. They also infused EMPs to live animal. In both cases, the EMPs caused further damage of endothelial function causing increased cell apoptosis (programmed death of cells), increased intracellular content of reactive oxygen species, decreased NO, increased cell permeability (leakage) and pro-inflammatory response.
The entire story of endothelial dysfunction and DCS sometimes is similar to the dilemma of chicken and egg: what is first, the bubbles that cause injury of endothelium, or the endothelial dysfunction that enhances occurrence of bubbles? This study verified that bubbles may cause endothelial injury but did not prove that it is the only possible scenario that occurs.
The same group presented another study that explored effects of endothelial protection on occurrence of DCS in animal model. They treated a group of animals with escin for seven days before dive exposure and compared outcomes in treated and in control group. Escin has been used for endothelial protection in various indications. In this experiment, animals that receive escin had less DCS and in case they got DCS the delay to onset of symptoms was longer and manifestations less severe. All other endothelial indices which they measured were improved.(2) The results support hypothesis that endothelial integrity is important for outcome of diving. However, this is not a proof that escin could be useful in protecting divers from DCS.
There were three studies presented that used FMD to measure decompression stress in divers. Nicolas Renne and coauthors presented measured FMD 30 to 140 minutes after dive to 30 m (98 ft) for 20 minutes in a deep pool with warm water. The dive was within no-decompression limits (but not likely without bubbles, which was not reported in the abstract). They have found borderline reduction of FMD at 30 and 70 minutes post-dive, with a complete recovery at 140 minutes.(3)
Jean Pierre Imbert and coauthors measured FMD before and after saturation diving. The decompression did not result in any bubbles but the FMD was still reduced in average for 7% with a complete recovery within 12 hours. These results support hypothesis that bubbles and FMD are two independent dimensions of decompression stress where bubbles result mainly from the changes in pressure while FMD reduction results from hyperoxia.(4)
The third paper uses FMD to study effects of nitrox after a dive to 25 msw (82 fsw) for 40 minutes. They found that in comparison to air, nitrox results in less bubbles, increased peripheral pulmonary resistance, and a reduction in FMD. Again, the bubbles and FMD appeared to be two independent indices of DCS. However, it was unusual in this study that diving air to 25 m (82 ft), which exposes divers to 0.74 ATA partial pressure of oxygen, did not change at all the FMD.(5)
Both EMPs and FMD remain promising in the study of mechanisms of decompression sickness and we hope that the presented work at EUBS will find their way into peer reviewed scientific journals.
- Xuaxu Yu, Jiaju Xu, Weigang Xu. Bubble-induced endothelial microparticles promote endothelial dysfunction. Abstract and Conference Book. 42nd Annual Scientific Meeting of the European Underwater and Baromedical Society. Geneva, Switzerland. 13-16 September, 2016;16
- Zhang Kunm Jiang Zhongxin, Ning Xiaowei, Weigang Xu. Protective effect of escin on decompression sickness in rats. Abstract and Conference Book. 42nd Annual Scientific Meeting of the European Underwater and Baromedical Society. Geneva, Switzerland. 13-16 September, 2016;63
- Renne N, et all. Flow mediated dilatation evolution after a Nemo33 scuba dive. Abstract and Conference Book. 42nd Annual Scientific Meeting of the European Underwater and Baromedical Society. Geneva, Switzerland. 13-16 September, 2016;83
- Imbert JP, Kiboub F, Balestra C. Measurement of the decompression stress during offshore saturation. Abstract and Conference Book. 42nd Annual Scientific Meeting of the European Underwater and Baromedical Society. Geneva, Switzerland. 13-16 September, 2016;33
- Andre Zenske at all. Is nitrox dangerous for the recreational divers? Abstract and Conference Book. 42nd Annual Scientific Meeting of the European Underwater and Baromedical Society. Geneva, Switzerland. 13-16 September, 2016;32