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Central Nervous System Oxygen Toxicity (CNS-OT) is one of the most harmful effects of Enriched Air Nitrox (EAN) diving. Protective factors of the Ketogenic Diet (KD) are antioxidant activity, the prevention of mitochondrial damage and anti-inflammatory mechanisms. We aimed to investigate if a short-term KD may reduce oxidative stress and inflammation during an hyperoxic dive. Samples from six overweight divers (mean ± SD, age: 55.2 ± 4.96 years; BMI: 26.7 ± 0.86 kg/m 2 ) were obtained a) before and after a dive breathing Enriched Air Nitrox and performing 20-minute mild underwater exercise, b) after a dive (same conditions) performed after 7 days of KD. We measured urinary 8-isoprostane and 8-OH-2-deoxyguanosine and plasmatic IL-1β, IL-6 and TNF-α levels. The KD was successful in causing weight loss (3.20 ± 1.31 Kgs, p < 0.01) and in limiting lipid peroxidation (3.63 ± 1.16 vs. 1.11 ± 0.22; p < 0.01) and inflammatory response (IL-1β = 105.7 ± 25.52 vs. 57.03 ± 16.32, p < 0.05; IL-6 = 28.91 ± 4.351 vs. 14.08 ± 1.74, p < 0.001; TNF-α = 78.01 ± 7.69 vs. 64.68 ± 14.56, p < 0.05). A short-term KD seems to be effective in weight loss, in decreasing inflammation and protective towards lipid peroxidation during hyperoxic diving.

Deep sea divers, aviators and astronauts are at risk of decompression sickness when the ambient pressure reductions exceed a critical threshold. Venous bubbles associated with decompression sickness have the potential to react with the vascular membrane and adjacent blood products, eliciting an inflammatory cascade. Preventive measures usually involve careful decompression procedures to avoid or reduce bubble formation. De-nitrogenation with 100% oxygen pre-breathing as a preventive measure has been well established at least in altitude decompression exposures. The objective of this study was to determine the physiological and biochemical effects of Hyperbaric Oxygen Pre-breathe (HBOP) upon decompression from a hyperbaric exposure. Male Sprague-Dawley rats were randomly assigned to one of eight groups. Two experimental groups received HBOP at 1 and 18 hours prior to decompression, as compared with ground level oxygen or non-treated groups that still experienced decompression stress, and the associated non-decompressed controls. The results showed decreased extravascular lung water (pulmonary edema), bronchoalveolar lavage and pleural protein and arterial, broncho-alveolar lavage, and urine leukotriene E4 (LKE4) levels in both the 1Hr and 18Hr HBOP decompressed rats compared to non-oxygenated decompressed rats, as well as a decreased overall expression of signs of decompression sickness. This study indicates that HBOP-treated rats exhibit fewer signs and complications of decompression sickness compared with non-treated or ground level oxygen treated rats.

Decompression-induced venous bubble formation has been linked to increased neutrophil counts, endothelial cell injury, release of vasoactive eicosanoids, and increased vascular membrane permeability. These actions may account for inflammatory responses and edema formation. Increasing the intracellular cAMP has been shown to decrease eicosanoid production and edema formation in various models of lung injury. Reduction of decompression-induced inflammatory responses was evaluated in decompressed rats pretreated with saline (controls) or dibutyryl cAMP (DBcAMP, an analog of cAMP). After pretreatment, rats were exposed to either 616 kPa for 120 min or 683 kPa for 60 min. The observed increases in extravascular lung water ratios (pulmonary edema), bronchoalveolar lavage, and pleural protein in the saline control group (683 kPa) were not evident with DBcAMP treatment. DBcAMP pretreatment effects were also seen with the white blood cell counts and the percent of neutrophils in the bronchoalveolar lavage. Urinary levels of thromboxane B2, 11-dehydrothromboxane B2, and leukotriene E4 were significantly increased with the 683 kPa saline control decompression exposure. DBcAMP reduced the decompression-induced leukotriene E4 production in the urine. Plasma levels of thromboxane B2, 11-dehydrothromboxane B2, and leukotriene E4 were increased with the 683-kPa exposure groups. DBcAMP treatment did not affect these changes. The 11-dehydrothromboxane B2 and leukotriene E4 levels in the bronchoalveolar lavage were increased with the 683 kPa exposure and were reduced with the DBcAMP treatment. Our results indicate that DBcAMP has the capability to reduce eicosanoid production and limit membrane permeability and subsequent edema formation in rats experiencing decompression sickness.