Decompression sickness (DCS) is a pathology caused by the appearance of gas emboli in the bloodstream and tissues. However, the weak correlation between the amount of venous gas emboli (VGE) and the development of DCS, as well as the considerable interindividual variability in DCS susceptibility, suggests that a higher DCS resistance could be associated with a better management of VGE-induced stress. To study the effects of VGE independently of the hyperbaric stress induced by diving, Wistar and DCS-resistant male and female rats received 5 mL/kg of a 0.9% NaCl solution containing air microbubbles through the tail vein. After 120 min, the liver and lungs were harvested. Wet-to-dry weight ratio was determined in the lungs. Gene expression was quantified by reverse transcription-polymerase chain reaction in the liver. Compared with standard Wistar, DCS-resistant rats exhibited a lower lung wet-to-dry weight ratio after air microbubble injection, suggesting lower pulmonary fluid accumulation. In the liver, DCS-resistant rats showed higher tissue factor transcription at the basal state and post-air microbubble injection. Tissue factor pathway inhibitor was lower in DCS-resistant rats at the basal state but higher following air microbubble injection. Levels of heat shock protein 70 (HSP70), heat shock protein 27 (HSP27), and early growth response 1 (Egr-1) were higher in DCS-resistant rats after air microbubble injection. At the basal state, only HSP27 was higher in DCS-resistant rats, with HSP70 lower and Egr-1 not different. These results help clarify the pathways involved in the response to VGE and highlight potential mechanisms underlying resistance to DCS, including enhanced anticoagulant pathways and improved cellular stress responses.NEW & NOTEWORTHY This study suggests for the first time that DCS resistance may be associated with a better tolerance to VGE. This greater DCS resistance could be achieved through improved control of the procoagulant effects of bubbles via TFPI-dependent inhibitory mechanisms and an enhanced cellular stress response to VGE by HSP70, HSP27, and EGR-1. It also suggests that it may be possible to stratify the individual DCS risk based on the thromboinflammatory response to bubbles.

Susceptibility to decompression sickness (DCS) shows wide interindividual variability, the origins of which remain poorly understood. To better elucidate its mechanisms, we previously developed a rat strain with more than threefold higher resistance to DCS through selective breeding. In this study, we examined baseline expression of genes related to antioxidant defense and mitochondrial biogenesis in the lungs and liver of DCS-resistant and nonresistant Wistar rats. None of the animals were exposed to hyperbaric conditions, allowing us to focus on constitutive expression differences potentially underlying genetic resistance to DCS. Quantitative reverse transcription polymerase chain reaction was performed, and data were analyzed using two-way ANOVA to assess the effects of selection, sex, and their interaction. In the lungs, no significant selection effect was observed for genes involved in mitochondrial biogenesis (Pgc1α, Nrf1, and Nrf2) or antioxidant defense (Sod1, Sod2, Gpx1, and Cat). In contrast, in the liver, expression of both gene groups was significantly decreased in resistant rats (P < 0.0083, Bonferroni correction), except for Pgc1α. These lower hepatic expression levels align with the previously reported reduction in citrate synthase activity and lower basal oxygen consumption in the soleus muscle of resistant rats. Together, these findings suggest that hepatic metabolism and mitochondrial function may play key roles in DCS susceptibility, potentially through reduced mitochondrial activity and lower reactive oxygen species production in resistant animals.NEW & NOTEWORTHY This study analyzed genes related to antioxidant defense and mitochondrial biogenesis in the lungs and liver of rats bred for resistance to decompression sickness (DCS). In resistant rats, no change was observed in lung gene expression, whereas both gene groups were downregulated in the liver (P < 0.0083, Bonferroni correction), except Pgc1α. These findings, along with previous ones, suggest that hepatic mitochondrial function and reduced reactive oxygen species production may contribute to DCS resistance.

Introduction Decompression sickness (DCS) is driven by gas bubble formation after scuba diving and a subsequent thromboinflammatory response. Extracellular vesicles (EV) and especially microparticles (MPs) have emerged as potential mediators of this response. While the physical properties of helium and nitrogen, two widely used inert respiratory gases, are well-documented, the biological impact on MPs release and content remains poorly understood. Objective This study aims to evaluate DCS outcomes and characterize MPs subtypes in a rat model using identical heliox and nitrox profiles. Method Male Sprague Dawley rats (n=12 per group) were subjected to simulated dives in a 40-liter hyperbaric chamber. Animals were compressed at 200kPa/min to a pressure of 700kPa for a bottom time of 90minutes. Decompression was conducted at 50kPa/min to atmospheric pressure. Two gas mixtures were compared: nitrox 21% (79% N2, 21% O2) and heliox 21% (79% He, 21% O2). Following decompression, rats were observed for 60minutes for clinical signs of DCS and blood was collected for the isolation of MPs. These rats were compared with controls rats exposed to the same gas at atmospheric pressure (n=6 per group). Characterization included flow cytometry for thromboinflammatory markers, including P-selectin, CD142, phalloidin, and thrombospondin. Results Experimental runs demonstrated a significant difference in DCS incidence between the two gas mixtures despite identical pressure-time profiles. Nitrox 21% dives resulted in a severe DCS rate of 83%, whereas heliox 21% dives resulted in a substantially lower rate of 33%. Preliminary flow cytometry results showed a significant decrease in MPs concentration in helium diving rats without DCS compared with helium controls (P=0.0317). This was associated with reduced proportions of CD142 (P=0.02214) and phalloidin positive MPs (P=0.01502). Following nitrogen exposure, DCS rats showed a trend toward increased MP concentration (P=0.0992), also nitrogen-exposed DCS rats exhibited a reduced proportion of thrombospondin-positive MPs (P=0.01931). Although preliminary results have already provided insights into MPs, further analyses, including their OMICS content (proteins, mRNA, miRNA), are ongoing to complete these findings. Conclusion In this rat model, helium-based decompression resulted in a lower incidence of DCS associated with a decrease in pro-inflammatory/coagulant MPs.

Introduction: Technical diving, involving rebreathers and/or helium-based gas mixtures for deeper and longer dives, may influence risk and clinical presentation of injuries due to helium's properties, equipment constraints, or exposure conditions. This study aims to describe the specific characteristics of this accidentology. Methods: A retrospective study was conducted across five French coastline hyperbaric units. Medical records of technical divers presenting with decompression sickness (DCS), immersion pulmonary oedema (IPO), or gas-toxicity between 2010 and 2024 were reviewed. Results: 127 technical divers were included, three declined participation, leaving 124 cases for analysis. DCS was the most frequent condition (n = 105) followed by IPO (n = 16) and gas toxicity (n = 3). Median age was 45 [IQR 37-53] years, and 113 (91%) were male. Rebreathers were used in 94 (75.8%) cases and helium-based mixtures in 77 (62%). Previous diving-related accidents were reported in 36 (29%) cases. IPO occurred mainly after shallower dives in wetsuits and was frequently associated with procedural errors. Among DCS cases isolated musculoskeletal DCS predominated (n = 36), whereas spinal involvement was less frequent. When indicated, median recompression delay was 238 [IQR 135-555] minutes. Unfavourable outcomes occurred in 26 (25%) DCS cases, primarily with bone or inner-ear involvement. Conclusions: Technical diving accidents exhibit distinct patterns from recreational diving, notably greater musculoskeletal involvement and a possible increased risk of dysbaric osteonecrosis (DON). Current evidence does not support different management, but the risk of potential initially silent bone lesions should not be overlooked. Further research on helium-related risks and hyperbaric treatment's role in DON prevention is needed.

Nitric oxide (NO) plays a crucial role in muscle oxidative capacity, which predicts muscle strength. This study aimed to investigate whether different breathing techniques (nasal or oral breathing) affect muscle performance during acute exhaustive exercise. In our study, 49 healthy individuals (24♀/25♂; age 22.8 ± 3.4 years) performed two Wingate anaerobic tests in a counterbalanced order. Although perceived exertion was significantly higher with oral breathing (Borg Scale: 9.0 ± 1.1 vs. 8.0 ± 1.3, p = 0.04), breathing mode did not impact power output (peak: 749 ± 290 vs. 728 ± 284 W; average: 576 ± 217 vs. 575 ± 216 W, p = 0.2). NIRS data indicated no significant differences in muscle desaturation between the two breathing modes; however, nasal breathing resulted in significantly faster (0.45 ± 0.4 vs. 0.23 ± 0.12%/s, p = 0.02) and greater (75.2 ± 4.0 vs. 73.1 ± 3.6%, p = 0.04) post-exercise muscle recovery. As an indirect marker of NO bioavailability, flow-mediated dilation (FMD) was associated with a significant improvement (Pre: 107.4 ± 3.0% vs. Post: 110.3 ± 3.6%, p < 0.001) via nasal breathing only, with a significant difference between the two breathing modes (p < 0.0001). Therefore, we suggest that the nitrate–nitrite–NO pathway enhances muscle energy and function, which highlights the importance of nasal breathing.

Introduction:The use of gas mixtures containing helium for deep recreational diving is increasingly common, involving complex logistics and decision-making compromises. The characteristics and inherent risks of this practice remain poorly documented. This study aims to provide an epidemiological inventory of practices and diving-related incidents within the technical diving community. Methods:An international online survey was disseminated on social networks targeting certified trimix divers. It collected demographic data, diving experience, and dive management practices, along with self-reported unusual symptoms, treatments, and outcomes following trimix dives. Results:A total of 558 questionnaires were analysed, predominantly from males (92%), mostly over 46 years old (61%), with high certification levels and recreational diving purposes. Forty-two percent reported one or more medical risk factors related to diving. Rebreather use was prevalent (79% at least occasionally). Decompression was primarily managed using compartmental models (85%) with gradient-factors adjustment. Dive planning varied significantly among individuals. Gas density at depth frequently exceeded the current recommendations. Ten percent had experienced symptoms suggestive of gas toxicity, mainly related to nitrogen narcosis. Thirty-six percent (199/558) reported experiencing, at least once, symptoms of diving-related incidents, with 61% (n = 121/199) expressing certainty. In 48% (120/261) of incidents involving decompression sickness (DCS) or breathing symptoms, no treatment was initiated. Among episodes involving DCS symptoms (n = 254), 42% received normobaric oxygen, and 23% sought medical advice, while 16% were treated with hyperbaric oxygen. Only 2.5% reported probable long-lasting sequelae. Conclusions:The diversity of practices highlights the lack of robust scientific data supporting them. The accident rate in mixed-gas diving may be higher than in typical scuba air diving, though mostly of mild severity. Treatment appears to be neglected despite divers' high knowledge levels. Continued research into decompression and the physiological effects of these dives is essential, along with ongoing awareness and education efforts in diving first aid within this exposed community.

Introduction Decompression sickness (DCS) is a systemic syndrome that can occur after a reduction of environmental pressure, forming bubbles in blood circulation and tissues. The onset of DCS is characterised by different mechanisms including the activation of inflammation and coagulation cascade. Although the contribution of bubbles in triggering DCS is undeniable, various studies seem to show that this stress is not the only one involved and hyperbaric stress seems to induce inflammation. Previous studies suggested that DCS resistance could be associated with an increased blood inflammatory capacity and that these resistance mechanisms could differ between males and females. Objective This study aims to compare, in vitro, the effect of hyperbaric exposure solely on leukocytes and platelet activation depending on sex and DCS susceptibility. Method We isolated leukocytes and platelets from the blood of 39 Wistar rats (21 males and 18 females). These cells were split into two groups: atmospheric pressure or hyperbaric protocol. Then, the cells were analysed by flow cytometry. The platelets and different sub-populations of leukocytes were identified, and their activation was analysed thanks to specific markers. 4 weeks later, the rats were exposed to the same hyperbaric protocol to distinguish DCS-sensitive animals from the resistant ones. Results The percentage variation study between cells stayed at atmospheric pressure and exposed to hyperbaric protocol shows that hyperbaric stress increased the proportion of activated monocytes (MHCII+/CD11b/c Low) in DCS-sensitive rats (P=0.021). The study of the leukocytes & platelets interaction shows that the DCS-sensitive rats have a higher proportion of linked leukocytes-platelets (P=0.049). The percentage variation shows that hyperbaric stress modifies the platelet-leukocyte expression of CD142 (P=0.018) and CD62P with a Sexe*Susceptibility interaction (P=0.0019). Regarding the leukocytes sub-population, we found a Sexe*Susceptibility interaction in the percentage variation of platelets-neutrophils CD62P+/CD11b/c+ (P=0.015). Conclusion Our study shows that hyperbaric stress induces a higher monocyte activation in DCS-sensitive rats linked to a greater inflammatory profile. It also points that this stress induces leukocytes-platelets interaction that differs according to gender and DCS susceptibility.

Objective: present transcutaneous carbon dioxide (CO2)—tcpCO2—monitors suffer from limitations which hamper their widespread use, and call for a new tcpCO2 measurement technique. However, the progress in this area is hindered by the lack of knowledge in transcutaneous CO2 diffusion. To address this knowledge gap, this study focuses on investigating the influence of skin temperature on two key skin properties: CO2 permeability and skin blood flow.Methods: a monocentric prospective exploratory study including 40 healthy adults was undertaken. Each subject experienced a 90 min visit split into five 18 min sessions at different skin temperatures—Non-Heated (NH), 35, 38, 41, and 44°C. At each temperature, custom sensors measured transcutaneous CO2 conductivity and exhalation rate at the arm and wrist, while Laser Doppler Flowmetry (LDF) assessed skin blood flow at the arm.Results: the three studied metrics sharply increased with rising skin temperature. Mean values increased from the NH situation up to 44°C from 4.03 up to 8.88 and from 2.94 up to 8.11 m·s−1 for skin conductivity, and from 80.4 up to 177.5 and from 58.7 up to 162.3 cm3·m−2·h−1 for exhalation rate at the arm and wrist, respectively. Likewise, skin blood flow increased elevenfold for the same temperature increase. Of note, all metrics already augmented significantly in the 35–38°C skin temperature range, which may be reached without active heating—i.e. only using a warm clothing.Conclusion: these results are extremely encouraging for the development of next-generation tcpCO2 sensors. Indeed, the moderate increase (× 2) in skin conductivity from NH to 44°C tends to indicate that heating the skin is not critical from a response time point of view, i.e. little to no skin heating would only result in a doubled sensor response time in the worst case, compared to a maximal heating at 44°C. Crucially, a skin temperature within the 35–38°C range already sharply increases the skin blood flow, suggesting that tcpCO2 correlates well with the arterial paCO2 even at such low skin temperatures. These two conclusions further strengthen the viability of non-heated tcpCO2 sensors, thereby paving the way for the development of wearable transcutaneous capnometers.

Susceptibility to decompression sickness (DCS) is characterized by a wide inter-individual variability, the origins of which are still poorly understood. We selectively bred rats with at least a 3-fold greater resistance to DCS than standard rats after 6 generations. In order to better understand DCS mechanisms, we compared the static genome expression of these resistant rats from the 10th generation to their counterparts of the initial non-resistant Wistar strain, by a microarray transcriptomic approach coupled and crossed with a PCR plates miRnome study. Thus, we identified differentially expressed genes on selected males and females, as well as gender differences in those genes, and we crossed these transcripts with the respective targets of the differentially expressed microRNAs. Our results highlight pathways involved in inflammatory responses, circadian clock, cell signaling and motricity, phagocytosis or apoptosis, and they confirm the importance of inflammation in DCS pathophysiology. Static hepatic gene expression of resistant rats crossed with their circulating miRnome highlight the role of inflammatory pathways in the susceptibility and pathophysiology of decompression sickness.

Decompression sickness can occur in divers even when recommended decompression procedures are followed. Furthermore, the physiological state of individuals can significantly affect bubbling variability. These informations highlight the need for personalized input to improve decompression in SCUBA diving. The main objective of this study is to propose a fundamental framework for a new approach to inert gas exchanges. A physiological model of oxygen delivery to organs and tissues has been built and adapted to nitrogen. The validation of the model was made by transferring the N2 to CO2. Under normobaric conditions (air breathing, oxygen breathing, and static apnea) and hyperbaric conditions, the O2 model replicates the reference physiological Po2 (Spearman correlation tests P < 0.001). The inert gas models can simulate inert gas partial pressures under normobaric and hyperbaric conditions. However, the lack of reference values prevents direct validation of this new model. Therefore, the N2 model has been transferred to CO2. The resulting CO2 model has been validated by comparing it with physiological reference values (Spearman correlation tests P < 0.01). The validity of the CO2 model constructed from the N2 model demonstrates the plausibility of this physiological model of inert gas exchanges. In the context of personalized decompression procedures, the proposed model is of significant interest as it enables the integration of physiological and morphological parameters (blood and respiratory flows, alveolo-capillary diffusion, respiratory and blood volumes, oxygen consumption rate, fat mass, etc.) into a model of nitrogen saturation/desaturation, in which oxygen and CO2 partial pressures can also be incorporated.NEW & NOTEWORTHY This is the first model of inert gas transport based on the physiology of respiratory gas. It was built for O2 delivery and validated against literature data; it was then transposed to N2 exchanges. The transposition procedure was checked by transposing the N2 model to CO2 (and validated against literature data). This model opens the possibility to integrate physiological and morphological inputs in a personalized decompression procedure in SCUBA diving.

Introduction: Diving decompression theory hypothesizes inflammatory processes as a source of micronuclei which could increase related risks. Therefore, we tested 10 healthy, male divers. They performed 6–8 dives with a maximum of two dives per day at depths ranging from 21 to 122 msw with CCR mixed gas diving.Methods: Post-dive VGE were counted by echocardiography. Saliva and urine samples were taken before and after each dive to evaluate inflammation: ROS production, lipid peroxidation (8-iso-PGF2), DNA damage (8-OH-dG), cytokines (TNF-α, IL-6, and neopterin).Results: VGE exhibits a progressive reduction followed by an increase (p < 0.0001) which parallels inflammation responses. Indeed, ROS, 8-iso-PGF2, IL-6 and neopterin increases from 0.19 ± 0.02 to 1.13 ± 0.09 μmol.min−1 (p < 0.001); 199.8 ± 55.9 to 632.7 ± 73.3 ng.mg−1 creatinine (p < 0.0001); 2.35 ± 0.54 to 19.5 ± 2.96 pg.mL−1 (p < 0.001); and 93.7 ± 11.2 to 299 ± 25.9 μmol·mol−1 creatinine (p = 0.005), respectively. The variation after each dive was held constant around 158.3% ± 6.9% (p = 0.021); 151.4% ± 5.7% (p < 0.0001); 176.3% ± 11.9% (p < 0.0001); and 160.1% ± 5.6% (p < 0.001), respectively.Discussion: When oxy-inflammation reaches a certain level, it exceeds hormetic coping mechanisms allowing second-generation micronuclei substantiated by an increase of VGE after an initial continuous decrease consistent with a depletion of “first generation” pre-existing micronuclei.

In this study, the metabolic responses of hypoxic breathing for 1 h to inspired fractions of 10% and 15% oxygen were investigated. To this end, 14 healthy nonsmoking subjects (6 females and 8 males, age: 32.2 ± 13.3 years old (mean ± SD), height: 169.1 ± 9.9 cm, and weight: 61.6 ± 16.2 kg) volunteered for the study. Blood samples were taken before, and at 30 min, 2 h, 8 h, 24 h, and 48 h after a 1 h hypoxic exposure. The level of oxidative stress was evaluated by considering reactive oxygen species (ROS), nitric oxide metabolites (NOx), lipid peroxidation, and immune-inflammation by interleukin-6 (IL-6) and neopterin, while antioxidant systems were observed in terms of the total antioxidant capacity (TAC) and urates. Hypoxia abruptly and rapidly increased ROS, while TAC showed a U-shape pattern, with a nadir between 30 min and 2 h. The regulation of ROS and NOx could be explained by the antioxidant action of uric acid and creatinine. The kinetics of ROS allowed for the stimulation of the immune system translated by an increase in neopterin, IL-6, and NOx. This study provides insights into the mechanisms through which acute hypoxia affects various bodily functions and how the body sets up the protective mechanisms to maintain redox homeostasis in response to oxidative stress.

Oxygen is a powerful trigger for cellular reactions and is used in many pathologies, including oxidative stress. However, the effects of oxygen over time and at different partial pressures remain poorly understood. In this study, the metabolic responses of normobaric oxygen intake for 1 h to mild (30%) and high (100%) inspired fractions were investigated. Fourteen healthy non-smoking subjects (7 males and 7 females; age: 29.9 ± 11.1 years, height: 168.2 ± 9.37 cm; weight: 64.4 ± 12.3 kg; BMI: 22.7 ± 4.1) were randomly assigned in the two groups. Blood samples were taken before the intake at 30 min, 2 h, 8 h, 24 h, and 48 h after the single oxygen exposure. The level of oxidation was evaluated by the rate of reactive oxygen species (ROS) and the levels of isoprostane. Antioxidant reactions were observed by total antioxidant capacity (TAC), superoxide dismutase (SOD), and catalase (CAT). The inflammatory response was measured using interleukin-6 (IL-6), neopterin, creatinine, and urates. Oxidation markers increased from 30 min on to reach a peak at 8 h. From 8 h post intake, the markers of inflammation took over, and more significantly with 100% than with 30%. This study suggests a biphasic response over time characterized by an initial "permissive oxidation" followed by increased inflammation. The antioxidant protection system seems not to be the leading actor in the first place. The kinetics of enzymatic reactions need to be better studied to establish therapeutic, training, or rehabilitation protocols aiming at a more targeted use of oxygen.

Long-term alterations of pulmonary function (mainly decreased airway conductance and capacity of the lungs to diffuse carbon monoxide (DLCO)) have been described after hyperbaric exposures. However, whether these alterations convey a higher risk for divers’ safety has never been investigated before. The purpose of the present pilot study was to assess whether decreased DLCO is associated with modifications of the physiological response to diving. In this case–control observational study, 15 “fit-to-dive” occupational divers were split into two groups according to their DLCO measurements compared to references values, either normal (control) or reduced (DLCO group). After a standardized 20 m/40 min dive in a sea water pool, the peak-flow, vascular gas emboli (VGE) grade, micro-circulatory reactivity, inflammatory biomarkers, thrombotic factors, and plasmatic aldosterone concentration were assessed at different times post-dive. Although VGE were recorded in all divers, no cases of decompression sickness (DCS) occurred. Compared to the control, the latency to VGE peak was increased in the DLCO group (60 vs. 30 min) along with a higher maximal VGE grade (p < 0.0001). P-selectin was higher in the DLCO group, both pre- and post-dive. The plasmatic aldosterone concentration was significantly decreased in the control group (−30.4 ± 24.6%) but not in the DLCO group. Apart from a state of hypocoagulability in all divers, other measured parameters remained unchanged. Our results suggest that divers with decreased DLCO might have a higher risk of DCS. Further studies are required to confirm these preliminary results.

Decompression sickness (DCS) with neurological disorders includes an inappropriate inflammatory response which degenerates slowly, even after the disappearance of the bubbles. There is high inter-individual variability in terms of the occurrence of DCS that could have been mastered by the selection and then the breeding of DCS-resistant rats. We hypothesized the selection of single-nucleotide polymorphisms (SNPs) linked to autoimmunity operated upon a generation of a DCS-resistant strain of rats. We used the candidate gene approach and targeted SNPs linked to the signaling cascade that directly regulates inflammation of innate immunity transiting by the Toll-like receptors. Twenty candidate SNPs were investigated in 36 standard rats and 33 DCS-resistant rats. For the first time, we identify a diplotype (i.e., with matched haplotypes)-when coinherited-that strengthens protection against DCS, which is not strictly homozygous and suggests that a certain tolerance may be considered. We deduced an ideal haplotype of six variants from it (MyD88_50-T, _49-A, _97-C coupled to NFKB_85-T, _69-T, _45-T) linked to the resistant phenotype. Four among the six identified variants are located in pre- and/or post-transcriptional areas regulating MyD88 or NFKB1 expression. Because of missense mutations, the other two variants induce a structural change in the NFKB1 protein complex including one damage alteration according to the Missense3D algorithm. In addition to the MyD88/NFKB1 haplotype providing rats with a strong resistance to DCS, this also highlights the importance that the immune response, here linked to the genetic heritage, can have in the development of DCS and offer a new perspective for therapeutic strategies.

Hyperbaric oxygen therapy (HBOT) is a therapeutical approach based on exposure to pure oxygen in an augmented atmospheric pressure. Although it has been used for years, the exact kinetics of the reactive oxygen species (ROS) between different pressures of hyperbaric oxygen exposure are still not clearly evidenced. In this study, the metabolic responses of hyperbaric hyperoxia exposures for 1 h at 1.4 and 2.5 ATA were investigated. Fourteen healthy non-smoking subjects (2 females and 12 males, age: 37.3 ± 12.7 years old (mean ± SD), height: 176.3 ± 9.9 cm, and weight: 75.8 ± 17.7 kg) volunteered for this study. Blood samples were taken before and at 30 min, 2 h, 24 h, and 48 h after a 1 h hyperbaric hyperoxic exposure. The level of oxidation was evaluated by the rate of ROS production, nitric oxide metabolites (NOx), and the levels of isoprostane. Antioxidant reactions were assessed through measuring superoxide dismutase (SOD), catalase (CAT), cysteinylglycine, and glutathione (GSH). The inflammatory response was measured using interleukine-6, neopterin, and creatinine. A short (60 min) period of mild (1.4 ATA) and high (2.5 ATA) hyperbaric hyperoxia leads to a similar significant increase in the production of ROS and antioxidant reactions. Immunomodulation and inflammatory responses, on the contrary, respond proportionally to the hyperbaric oxygen dose. Further research is warranted on the dose and the inter-dose recovery time to optimize the potential therapeutic benefits of this promising intervention.

INTRODUCTION:Susceptibility to decompression sickness (DCS) is characterised by a wide inter-individual variability whose origins are still poorly understood. This hampers reliable prediction of DCS by decompression algorithms. We previously selectively bred rats with a 3-fold greater resistance to DCS than standard rats. Based on its previously reported relation with decompression outcomes, we assessed whether modification in vascular function is associated with resistance to DCS. METHODS:The arterial pressure response to intravenous administration of acetylcholine (ACh, 5 μg.kg-1) and adrenaline (5 and 10 μg.kg-1) was compared in anaesthetised DCS-resistant rats (seven females, seven males) and standard Wistar rats (seven females, 10 males) aged 14-15 weeks. None of these rats had previously undergone hyperbaric exposure. RESULTS:There was a non-significant tendency for a lower diastolic (DBP) and mean blood pressure (MBP) in DCS-resistant rats. After ACh administration, MBP was significantly lower in resistant rats, for both males (P = 0.007) and females (P = 0.034). After administration of adrenaline 10 μg.kg-1, DCS-resistant rats exhibited lower maximal DBP (P = 0.016) and MBP (P = 0.038). Systolic and pulse blood pressure changes did not differ between groups in any of the experiments. CONCLUSIONS:Resistance to DCS in rats is associated to a trend towards a lower vascular tone but not blood pressure reactivity. Whether these differences are a component of the susceptibility to DCS remains to be confirmed.

EDITORIAL article Front. Physiol., 17 March 2022Sec.Environmental, Aviation and Space Physiology https://doi.org/10.3389/fphys.2022.870917