Underwater

Author(s):  
Chris Johnson ◽  
Robert Conway ◽  
Lesley F. Thomson ◽  
Andy Pitkin ◽  
Rose Drew

The underwater environment - Preparations before travel - Diving medicine - Effects of high-pressure gases - Decompression sickness - Barotrauma - Other problems

Author(s):  
Chris Johnson ◽  
Robert Conway ◽  
Lesley F. Thomson ◽  
Andy Pitkin ◽  
Rose Drew

The underwater environment - Preparations before travel - Diving medicine - Effects of high-pressure gases - Decompression sickness - Barotrauma - Other problems


Author(s):  
Veena M. Bhopale ◽  
Deepa Ruhela ◽  
Kaighley D. Brett ◽  
Nathan Z. Nugent ◽  
Noelle K. Fraser ◽  
...  

Plasma gelsolin (pGSN) levels fall in association with diverse inflammatory conditions. We hypothesized pGSN would decrease due to the stresses imposed by high pressure and subsequent decompression, and repletion would ameliorate injuries in a murine decompression sickness (DCS) model. Research subjects were found to exhibit a modest decrease in pGSN level while at high pressure and a profound decrease after decompression. Changes occurred concurrent with elevations of circulating microparticles (MPs) carrying interleukin (IL)-1β. Mice exhibited a comparable decrease in pGSN after decompression along with elevations of MPs carrying IL-1β. Infusion of recombinant human (rhu)-pGSN into mice before or after pressure exposure abrogated these changes and prevented capillary leak in brain and skeletal muscle. Human and murine MPs generated under high pressure exhibited surface filamentous (F-) actin to which pGSN binds, leading to particle lysis. Additionally, human neutrophils exposed to high air pressure exhibit an increase in surface F-actin that is diminished by rhu-pGSN resulting in inhibition of MPs production. Administration of rhu-pGSN may have benefit as prophylaxis or treatment for DCS.


1965 ◽  
Vol 20 (5) ◽  
pp. 927-933 ◽  
Author(s):  
Hugh D. Van Liew ◽  
Beverly Bishop ◽  
Pio Walder D. ◽  
Hermann Rahn

Data with subcutaneous gas pockets in rats and theoretical considerations lead to the following conclusions concerning the effects of compression on preformed gas bubbles in the body: 1) Besides mechanically decreasing bubble size, compression causes an additional volume decrease due to readjustment of water vapor, CO2 and O2 volumes in the bubble. 2) The pocket-to-tissue Pn2 difference (in the stabilized condition in which tissue Pn2 equals arterial Pn2) is almost completely dependent on alveolar oxygen, not on compression per se. Compression with air elevates alveolar O2, but the same nitrogen difference could be gained by inhaling oxygen-enriched gas at lower pressures. 3) Compression causes an increased pocket-to-tissue Pn2 difference which hastens N2 absorption, but at the same time decreases surface area and thus tends to slow absorption. hyperbaric; oxygen; decompression sickness; gas bubbles; high pressure Submitted on October 26, 1964


2007 ◽  
Vol 102 (4) ◽  
pp. 1324-1328 ◽  
Author(s):  
R. Arieli ◽  
P. Svidovsky ◽  
A. Abramovich

Trimix (a mixture of helium, nitrogen, and oxygen) has been used in deep diving to reduce the risk of high-pressure nervous syndrome during compression and the time required for decompression at the end of the dive. There is no specific recompression treatment for decompression sickness (DCS) resulting from trimix diving. Our purpose was to validate a rat model of DCS on decompression from a trimix dive and to compare recompression treatment with oxygen and heliox (helium-oxygen). Rats were exposed to trimix in a hyperbaric chamber and tested for DCS while walking in a rotating wheel. We first established the experimental model, and then studied the effect of hyperbaric treatment on DCS: either hyperbaric oxygen (HBO) (1 h, 280 kPa oxygen) or heliox-HBO (0.5 h, 405 kPa heliox 50%-50% followed by 0.5 h, 280 kPa oxygen). Exposure to trimix was conducted at 1,110 kPa for 30 min, with a decompression rate of 100 kPa/min. Death and most DCS symptoms occurred during the 30-min period of walking. In contrast to humans, no permanent disability was found in the rats. Rats with a body mass of 100–150 g suffered no DCS. The risk of DCS in rats weighing 200–350 g increased linearly with body mass. Twenty-four hours after decompression, death rate was 40% in the control animals and zero in those treated immediately with HBO. When treatment was delayed by 5 min, death rate was 25 and 20% with HBO and heliox, respectively.


2004 ◽  
Vol 287 (5) ◽  
pp. R1214-R1218 ◽  
Author(s):  
Chien-Ling Su ◽  
Chin-Pyng Wu ◽  
Shao-Yuan Chen ◽  
Bor-Hwang Kang ◽  
Kun-Lun Huang ◽  
...  

Diving acclimatization refers to a reduced susceptibility to acute decompression sickness (DCS) in individuals undergoing repeated compression-decompression cycles. We demonstrated in a previous study that the mechanism responsible for this acclimatization is similar to that of stress preconditioning. In this study, we investigated the protective effect of prior DCS preconditioning on the severity of neurological DCS in subsequent exposure to high pressure in rabbits. We exposed the rabbits ( n = 10) to a pressure cycle of 6 absolute atmospheres (ATA) for 90 min, which induced signs of neurological DCS in 60% of the animals. Twenty-four hours after the pressure cycle, rabbits with DCS expressed more heat-shock protein 70 (HSP70) in the lungs, liver, and heart than rabbits without signs of disease or those in the control group ( n = 6). In another group of rabbits ( n = 24), 50% of animals presented signs of neurological DCS after exposure to high pressure, with a neurological score of 46.5 (SD 19.5). A course of hyperbaric oxygen therapy alleviated the signs of neurological DCS and ensured the animals' survival for 24 h. Experiencing another pressure cycle of 6 ATA for 90 min, 50% of 12 rabbits with prior DCS preconditioning developed signs of DCS, with a neurological score of 16.3 (SD 28.3), significantly lower than that before hyperbaric oxygen therapy ( P = 0.002). In summary, our results show that the occurrence of DCS in rabbits after rapid decompression is associated with increased expression of a stress protein, indicating that the stress response is induced by DCS. This phenomenon was defined as “DCS preconditioning.” DCS preconditioning attenuated the severity of neurological DCS caused by subsequent exposure to high pressure. These results suggest that bubble formation in tissues activates the stress response and stress preconditioning attenuates tissue injury on subsequent DCS stress, which may be the mechanism responsible for diving acclimatization.


2021 ◽  
Vol 8 ◽  
Author(s):  
Alicia Velázquez-Wallraf ◽  
Antonio Fernández ◽  
Maria José Caballero ◽  
Andreas Møllerløkken ◽  
Paul D. Jepson ◽  
...  

Decompression sickness (DCS) is a widely known clinical syndrome in human medicine, mainly in divers, related to the formation of intravascular and extravascular gas bubbles. Gas embolism and decompression-like sickness have also been described in wild animals, such as cetaceans. It was hypothesized that adaptations to the marine environment protected them from DCS, but in 2003, decompression-like sickness was described for the first time in beaked whales, challenging this dogma. Since then, several episodes of mass strandings of beaked whales coincidental in time and space with naval maneuvers have been recorded and diagnosed with DCS. The diagnosis of human DCS is based on the presence of clinical symptoms and the detection of gas embolism by ultrasound, but in cetaceans, the diagnosis is limited to forensic investigations. For this reason, it is necessary to resort to experimental animal models to support the pathological diagnosis of DCS in cetaceans. The objective of this study is to validate the pathological results of cetaceans through an experimental rabbit model wherein a complete and detailed histopathological analysis was performed. Gross and histopathological results were very similar in the experimental animal model compared to stranded cetaceans with DCS, with the presence of gas embolism systemically distributed as well as emphysema and hemorrhages as primary lesions in different organs. The experimental data reinforces the pathological findings found in cetaceans with DCS as well as the hypothesis that individuality plays an essential role in DCS, as it has previously been proposed in animal models and human diving medicine.


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