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Miroslav Rozloznik
added 2 research items
Vascular gas bubbles are considered the principal element in decompression sickness (DCS) development. Traditionally these bubbles were called VGE (venous gas emboli), however scientific knowledge indicates that similar bubbles may also be present in the arterial circulation, therefore we propose to use “VGE” for “Vascular Gas Emboli”, and we will do so throughout the text. Reduction of VGE production represents an interesting endpoint to decrease decompression stress and DCS risk. Here we will discuss state of the art pre-dive techniques and approaches, commonly known as preconditioning, used to reduce post-dive VGE load and decompression stress. Evidence based approaches clearly show that some types of preconditioning are more potent in VGE reduction, some indecompression stress reduction and there are some with a positive impact on both. Nevertheless, further research is required to investigate the mechanisms underlying these positive effects.
Decompression sickness (DCS) in divers is caused by bubbles of inert gas. When DCS occurs, most bubbles can be found in the venous circulation: venous gas emboli (VGE). Bubbles are thought to be stabilized by low molecular weight surfactant reducing the plasma-air surface tension (γ). Proteins may play a role as well. We studied the interrelations between these substances, γ and VGE, measured before and after a dry dive simulation. VGE of 63 dive simulations (21-msw/40-minute profile) of 52 divers was examined 40, 80, 120 and 160 minutes after surfacing (precordial Doppler method) and albumin, total protein, triglycerides, total cholesterol and free fatty acids were determined pre-and post-exposure. To manipulate blood plasma composition, half of the subjects obtained a fat-rich breakfast, while the other half got a fat-poor breakfast pre-dive. Eleven subjects obtained both. VGE scores measured with the precordial Doppler method were transformed to the logarithm of Kisman Integrated Severity Scores. With statistical analysis, including (partial) correlations, it could not be established whether γ as well as VGE scores are related to albumin, total protein or total cholesterol. With triglycerides and fatty acids correlations were also lacking, despite the fact that these compounds varied substantially. The same holds true for the paired differences between the two exposures of the 11 subjects. Moreover, no correlation between surface tension and VGE could be shown. From these findings and some theoretical considerations it seems likely that proteins lower surface tension rather than lipids. Since the findings are not in concordance with the classical surfactant hypothesis, reconsideration seems necessary.