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

The small angle tile calorimeter in the DELPHI experiment

The {\bf S}mall angle {\bf TI}le {\bf C}alorimeter ({\bf STIC}) provides calorimetric coverage in the very forward region of the DELPHI experiment at the CERN LEP collider. The structure of the calorimeters, built with a so-called ``shashlik'' technique, gives a perfectly hermetic calorimeter and still allows for the insertion of tracking detectors within the sampling structure to measure the direction of the showering particle. A charged-particle veto system, composed of two scintillator layers, makes it possible to trigger on single photon events and provides e-$\gamma$ separat ion. Results are presented from the extensive studies of these detectors in the CERN testbeams prior to installation and of the detector performance at LEP

Endothelial dysfunction correlates with decompression bubbles in rats

© 2016 The Author(s). Previous studies have documented that decompression led to endothelial dysfunction with controversial results. This study aimed to clarify the relationship between endothelial dysfunction, bubble formation and decompression rate. Rats were subjected to simulated air dives with one of four decompression rates: one slow and three rapid. Bubble formation was detected ultrasonically following decompression for two hours, before measurement of endothelial related indices. Bubbles were found in only rapid-decompressed rats and the amount correlated with decompression rate with significant variability. Serum levels of ET-1, 6-keto-PGF1a, ICAM-1, VCAM-1 and MDA, lung Wet/Dry weight ratio and histological score increased, serum NO decreased following rapid decompression. Endothelial-dependent vasodilatation to Ach was reduced in pulmonary artery rings among rapid-decompressed rats. Near all the above changes correlated significantly with bubble amounts. The results suggest that bubbles may be the causative agent of decompression-induced endothelial damage and bubble amount is of clinical significance in assessing decompression stress. Furthermore, serum levels of ET-1 and MDA may serve as sensitive biomarkers with the capacity to indicate endothelial dysfunction and decompression stress following dives