The mechanisms by which bubbles produce the clinical syndrome of decompression illness (DCI) continue to receive attention. Building on previously published work from the lab of Steven Thom (Institute for Environmental Medicine, PA, USA), a number of groups presented a work further defining the role of endothelial and neutrophil activation, and the interaction of a range of immune mediators. The protective effect of hyperbaric oxygen preconditioning prior to decompression stress via heat shock proteins, as demonstrated in a rat model by Wang Xu (Faculty of Naval Medicine, Shanghai, China), further confirms the ability of hyperbaric oxygen exposure to induce anti-oxidant and anti-apoptotic effects. Thom demonstrated the production of pro-inflammatory micro particles (MPs) in the plasma of human volunteers, having previously demonstrated that the injection of such particles into naive mice reproduced the vascular injury associated with DCI. Interestingly, Thom was unable to show a positive correlation between the number of MPs and bubble numbers in the human volunteers, although there was such a correlation with β-2 integrin expression (an indication of platelet-neutrophil interactions), previously used as an index of decompression stress.
Fang and Bao (Institute of Naval Medical Research, Shanghai, China) similarly demonstrated elevated levels of circulating inflammatory cytokines after a provocative decompression, including IFN-γ, TNF-α and IL-6. These changes were associated with the activation of mitogen-activated protein kinase pathways – further evidence of the importance of the bubble-endothelium interactions that result in clinical symptoms of DCI.
The recent interest in the mechanism of swimming-induced pulmonary oedema has been generated by a number of reports of deaths in the diving population where pulmonary oedema on surfacing seemed the likely cause. This phenomenon received considerable attention at the meeting. Richard Moon (Duke University Medical Center, Durham, NC, USA) investigated 20 volunteers using transthoracic echocardiography during head-out immersion exercise in cold water. He confirmed a progressive increase in pulmonary artery pressure during the exercise period and concluded that this was most likely due to the decreased left ventricular compliance. We are getting closer to understanding how very fit young naval diving recruits can develop pulmonary oedema while maximally exercising in the water.