Infammatory response to hyperbaric trauma. An experimental and clinical study

Reductions in ambient pressure liberates gas in various tissues and can result in decompression illness. In this thesis the patophysiological implications of a blood gas interface resulting from decompression was investigated with reference to the influence on biochemical mediators of inflammation. In a series of experiments, animals and human subjects have been exposed to hyperbaric trauma of different severity and duration. The hyperbaric exposures were performed using a dry decompression chamber and in open water dives. Post dive bubbledetection in the venous circulation was performed using echocardiography and levels of inflammatory mediators were analysed. The main results and conclusions were : • Dives in accordance with normal diving tables produces intravascular bubbles in the venous circulation, not necessarily correlated to clinical symptoms of DCS. Bubbles can be detected for as long as 16 h post dive. • A verified blood - gas interface after decompression seems capable of activating inflammatory cells and pro-inflammatory mediators as well as to stimulate an anti-inflammatory counter- response in a dose dependent fashion. • The magnitude of the systemic pro inflammatory response seem to correlate to the severity of the hyperbaric trauma in that way that only a trauma severe enough to cause profound clinical DCS resulted in systemic significant levels of proinflammatory mediators. • The response of an acute hyperbaric trauma were found to be different from a repetitive one in respect of the anti-inflammatory response, suggesting an adaptation mechanism of the anti-inflammatory system. • The findings presented in this thesis are consistent with different levels of activation of the inflammatory system. It is plausible that the bubble formation during decompression is the trigger of this inflammatory response. It is therefore suggested that the interplay between pro- and anti-inflammatory substances is a fine-tuned balance-act and it is only when this balance collapses that morbidity ensues. • The inflammatory interplay demonstrated in this thesis suggests an inflammatory mechanism as part of the pathogenesis in DCS