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

A new model of head-up display dive computer addressing safety-critical rate of ascent and returning gas pressure - A pilot trial

Head up displays (HUD) are beneficial in diving situations when the diver uses both hands for an activity, e.g. photography, scientific work, operating a diver propulsion vehicle or during diver training. They remove the need to locate a submersible pressure gauge or remember to look at a personal dive computer. A new model of HUD, one that can easily be retrospectively fitted to a recreational diver's regulator hose outside the mask lens, has been developed. A pilot study of 93 open circuit recreational dives was conducted over one week in Croatia, to assess the HUD-user interface. An electronic survey was developed and completed twice after 16 dives. Mean maximum depth was 23 m and mean total dive time 38 mins. 34 dives (37%) were made with the HUD and 59 made with traditional submersible pressure gauges. There was good test-retest agreement (kappa score=0.9) between repeated surveys. The HUD was relatively easy to attach and could be operated without the necessity of reading the user manual. The HUD has two potential mechanisms for preventing rapid ascent injuries. Firstly, displaying an ascent rate warning directly in the divers' field of vision and, secondly, by reducing the likelihood of an out-of-gas situation

Development of a personificated registration in a wireless network system

Mūsu laikos lielu popularitāti ir ieguvuši portatīvie datori un citas mobilās ierīces, ar kuru palīdzību var izmantot Interneta resursus. Tādēļ pašlaik daudzās publiskās vietās ir iespēja lietot bezvadu tīklu, kurš dod piekļuvi Internētam . Šī sistēma ir izstrādāta Interneta lietotāju kontrolei publiskās vietās.In our time great popularity obtained portable computers and other mobile devices that makes possible to use the resources of the Internet. Therefore now there is possibility to use a wireless network which gives access in the Internet in many public places. This system is developed for control of user of the Internet in public places

Endothelia-targeting protection by Escin in decompression sickness rats

© The Author(s) 2017. Endothelial dysfunction is involved in the pathogenesis of decompression sickness (DCS) and contributes substantively to subsequent inflammatory responses. Escin, the main active compound in horse chestnut seed extract, is well known for its endothelial protection and anti-inflammatory properties. This study aimed to investigate the potential protection of escin against DCS in rats. Escin was administered orally to adult male rats for 7 d (1.8 mg/kg/day) before a simulated air dive. After decompression, signs of DCS were monitored, and blood and pulmonary tissue were sampled for the detection of endothelia related indices. The incidence and mortality of DCS were postponed and decreased significantly in rats treated with escin compared with those treated with saline (P < 0.05). Escin significantly ameliorated endothelial dysfunction (increased serum E-selectin and ICAM-1 and lung Wet/Dry ratio, decreased serum NO), and oxidative and inflammatory responses (increased serum MDA, MPO, IL-6 and TNF-a) (P < 0.05 or P < 0.01). The results suggest escin has beneficial effects on DCS related to its endothelia-protective properties and might be a drug candidate for DCS prevention and treatment

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