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To test the hypothesis whether enriched air nitrox (EAN) breathing during simulated diving reduces decompression stress when compared to compressed air breathing as assessed by intravascular bubble formation after decompression. Human volunteers underwent a first simulated dive breathing compressed air to include subjects prone to post-decompression venous gas bubbling. Twelve subjects prone to bubbling underwent a double-blind, randomized, cross-over trial including one simulated dive breathing compressed air, and one dive breathing EAN (36% O2) in a hyperbaric chamber, with identical diving profiles (28 msw for 55 minutes). Intravascular bubble formation was assessed after decompression using pulmonary artery pulsed Doppler. Twelve subjects showing high bubble production were included for the cross-over trial, and all completed the experimental protocol. In the randomized protocol, EAN significantly reduced the bubble score at all time points (cumulative bubble scores: 1 [0-3.5] vs. 8 [4.5-10]; P < 0.001). Three decompression incidents, all presenting as cutaneous itching, occurred in the air versus zero in the EAN group (P = 0.217). Weak correlations were observed between bubble scores and age or body mass index, respectively. EAN breathing markedly reduces venous gas bubble emboli after decompression in volunteers selected for susceptibility for intravascular bubble formation. When using similar diving profiles and avoiding oxygen toxicity limits, EAN increases safety of diving as compared to compressed air breathing. ISRCTN 31681480.

Decompression sickness is a fatal disease worldwide. Therefore, to find a prophylactic modality for decompression sickness is urgently required. Bone marrow derived mesenchymal stem cells exhibit effectiveness in antioxidant, anti-inflammation, and decrease cell death; while its effects on decompression sickness remains unclear. This study aimed to further investigate the mechanisms of decompression sickness induced lung injury, as well as effects of bone marrow derived mesenchymal stem cells on decompression sickness induced lung injury and explore the role of oxidative stress, inflammation and cell death play in this disease. The study involved Sprague-Dawley rats age at 8−10 weeks weighting 350 ± 10g. Acute lung injury was induced by decompression hyperbaric chamber. A dose of bone marrow derived mesenchymal stem cells (2 × 10 6 cells) was given to rats one day prior to the start of decompression. Lung injury severity was estimated by determining lung damage scores, pulmonary oxidative, inflammatory factors and cell death. In bone marrow derived mesenchymal stem cells treated rats, the morbidity and mortality of decompression markedly decreased. The increases of protein IL-1 and IL-6 in BALF and lung wet/dry ratio and lung injury score were alleviated. The ROS, CAT, SOD, and MDA activities and GSH levels were significant attenuated (P < 0.05). The pyroptosis and nerroptosis were significant mitigate (P < 0.05). Based on the results, bone marrow derived mesenchymal stem cells is an potential efficient and safe prophylactic modality protect rats from decompression induced acute lung injury.

Diving air-breathing vertebrates have long been considered protected against decompression sickness (DCS) through anatomical, physiological, and behavioural adaptations. However, an acute systemic gas and fat embolic syndrome similar to DCS in human divers was described in beaked whales that stranded in temporal and spatial association with military exercises involving high-powered sonar. More recently, DCS has been diagnosed in bycaught sea turtles. Both cases were linked to human activities. Two Risso’s dolphin ( Grampus griseus ) out of 493 necropsied cetaceans stranded in the Canary Islands in a 16-year period (2000–2015), had a severe acute decompression sickness supported by pathological findings and gas analysis. Deadly systemic, inflammatory, infectious, or neoplastic diseases, ship collision, military sonar, fisheries interaction or other type of lethal inducing associated trauma were ruled out. Struggling with a squid during hunting is discussed as the most likely cause of DCS.

A 42-year-old man presented to the emergency department with skin changes, arthralgias, and vomiting after scuba diving. He was treated for decompression sickness.

Production of blood-borne microparticles (MPs), 0.1–1 µm diameter vesicles, and interleukin (IL)-1β in response to high pressure is reported in lab animals and associated with pathological changes. It is unknown whether the responses occur in humans, and whether they are due to exposure to high pressure or to the process of decompression. Blood from research subjects exposed in hyperbaric chambers to air pressure equal to 18 meters of sea water (msw) for 60 minutes or 30 msw for 35 minutes were obtained prior to and during compression and 2 hours post-decompression. MPs and intra-particle IL-1β elevations occurred while at pressure in both groups. At 18 msw (n = 15) MPs increased by 1.8-fold, and IL-1β by 7.0-fold (p < 0.05, repeated measures ANOVA on ranks). At 30 msw (n = 16) MPs increased by 2.5-fold, and IL-1β by 4.6-fold (p < 0.05), and elevations persisted after decompression with MPs elevated by 2.0-fold, and IL-1β by 6.0-fold (p < 0.05). Whereas neutrophils incubated in ambient air pressure for up to 3 hours ex vivo did not generate MPs, those exposed to air pressure at 180 kPa for 1 hour generated 1.4 ± 0.1 MPs/cell (n = 8, p < 0.05 versus ambient air), and 1.7 ± 0.1 MPs/cell (p < 0.05 versus ambient air) when exposed to 300 kPa for 35 minutes. At both pressures IL-1β concentration tripled (p < 0.05 versus ambient air) during pressure exposure and increased 6-fold (p < 0.05 versus ambient air) over 2 hours post-decompression. Platelets also generated MPs but at a rate about 1/100 that seen with neutrophils. We conclude that production of MPs containing elevated concentrations of IL-1β occur in humans during exposure to high gas pressures, more so than as a response to decompression. While these events may pose adverse health threats, their contribution to decompression sickness development requires further study.

Was sonar responsible for a spate of whale deaths after an Atlantic military exercise? There are spatial and temporal links between some mass strandings of cetaceans — predominantly beaked whales — and the deployment of military sonar 1 , 2 , 3 . Here we present evidence of acute and chronic tissue damage in stranded cetaceans that results from the formation in vivo of gas bubbles, challenging the view that these mammals do not suffer decompression sickness. The incidence of such cases during a naval sonar exercise indicates that acoustic factors could be important in the aetiology of bubble-related disease and may call for further environmental regulation of such activity.

Massive bubble formation after diving can lead to decompression sickness (DCS) that can result in central nervous system disorders or even death. Bubbles alter the vascular endothelium and activate blood cells and inflammatory pathways, leading to a systemic pathophysiological process that promotes ischemic damage. Fluoxetine, a well-known antidepressant, is recognized as having anti-inflammatory properties at the systemic level, as well as in the setting of cerebral ischemia. We report a beneficial clinical effect associated with fluoxetine in experimental DCS. 91 mice were subjected to a simulated dive at 90 msw for 45 min before rapid decompression. The experimental group received 50 mg/kg of fluoxetine 18 hours before hyperbaric exposure (n = 46) while controls were not treated (n = 45). Clinical assessment took place over a period of 30 min after surfacing. At the end, blood samples were collected for blood cells counts and cytokine IL-6 detection. There were significantly fewer manifestations of DCS in the fluoxetine group than in the controls (43.5% versus 75.5%, respectively; p = 0.004). Survivors showed a better and significant neurological recovery with fluoxetine. Platelets and red cells were significantly decreased after decompression in controls but not in the treated mice. Fluoxetine reduced circulating IL-6, a relevant marker of systemic inflammation in DCS. We concluded that fluoxetine decreased the incidence of DCS and improved motor recovery, by limiting inflammation processes.

Despite state-of-the-art hyperbaric oxygen (HBO) treatment, about 30% of patients suffering neurologic decompression sickness (DCS) exhibit incomplete recovery. Since the mechanisms of neurologic DCS involve ischemic processes which result in excitotoxicity, it is likely that HBO in combination with an anti-excitotoxic treatment would improve the outcome in patients being treated for DCS. Therefore, in the present study, we investigated the effect of the noble gas xenon in an ex vivo model of neurologic DCS. Xenon has been shown to provide neuroprotection in multiple models of acute ischemic insults. Fast decompression compared to slow decompression induced an increase in lactate dehydrogenase (LDH), a well-known marker of sub-lethal cell injury. Post-decompression administration of xenon blocked the increase in LDH release induced by fast decompression. These data suggest that xenon could be an efficient additional treatment to HBO for the treatment of neurologic DCS.

Study design: A prospective, animal model for pharmacological intervention of decompression sickness (DCS), including spinal cord (SC) injury. Background: Signs and symptoms of DCS can include joint pain, skin discoloration, cardiopulmonary congestion and SC injury; severity ranges from trivial to fatal. Non-recompressive therapy for DCS may improve time-to-treatment and therefore impact mortality and morbidity. Objectives: Oxycyte at 5 cc kg −1 provides both SC protection and statistically significant survival benefit in a swine model of DCS. The purpose of this study was to test whether a reduced dose of Oxycyte (3 cc kg −1 ) would provide similar benefit. Setting: Silver Spring, MD, USA Methods: Male Yorkshire swine ( N =50) underwent a non-linear compression profile to 200 fsw (feet of sea water), which was identical to previous work using the 5 cc kg −1 dose of Oxycyte. After 31 min of bottom time, decompression was initiated at 30 fsw per minute until surface pressure was reached. Following decompression and the onset of DCS, intravenous Oxycyte or saline was administered with concurrent 100% O 2 for 1 h. The primary end point was DCS-induced mortality, with Tarlov score and SC histopathology as secondary end points. Results: Oxycyte administration of 3 cc kg −1 following surfacing produced no significant detectable survival benefit. Animals that received Oxycyte, however, had reduced SC lesion area. Conclusion: Further studies to determine the lowest fully efficacious dose of Oxycyte for the adjunct treatment of DCS are warranted.

The investigation of deaths that involve diving using a compressed breathing gas (SCUBA diving) is a specialized area of forensic pathology. Diving related deaths occur more frequently in certain jurisdictions, but any medical examiner or coroner’s office may be faced with performing this type of investigation. In order to arrive at the correct conclusion regarding the cause and manner of death, forensic pathologists and investigators need to have a basic understanding of diving physiology, and should also utilize more recently developed technology and ancillary techniques. In the majority of diving related deaths, the cause of death is drowning, but this more often represents a final common pathway due to a water environment. The chain of events leading to the death is just as important to elucidate if similar deaths are to be minimized in the future. Re-enactment of accident scenarios, interrogation of dive computers, postmortem radiographic imaging, and slight alterations in autopsy technique may allow some of these diving related deaths to the better characterized. The amount and location of gas present in the body at the time of autopsy may be very meaningful or may simply represent a postmortem artifact. Medical examiners, coroners, and forensic investigators should consider employing select ancillary techniques to more thoroughly investigate the factors contributing a death associated with SCUBA diving.