Skin temperature influence on transcutaneous carbon dioxide (CO2) conductivity and skin blood flow in healthy human subjects at the arm and wrist.

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.

Can selenium-enriched spirulina supplementation ameliorate sepsis outcomes in selenium-deficient animals?

In intensive care units, sepsis is the first cause of death. In this pathology, inflammation and oxidative status play a crucial role in patient outcomes. Interestingly, 92% of septic patients exhibit low selenium plasma concentrations (a component of antioxidant enzymes). Moreover, Spirulina platensis, a blue-green algae, demonstrated anti-inflammatory effects. In this context, the main purpose of our study was to analyze the effect of a selenium-enriched spirulina after a selenium deficiency on sepsis outcome in rats. Sixty-four rats were fed 12 weeks with a selenium-deficient food. After 8 weeks, rats were supplemented (via drinking water) for 4 weeks with sodium selenite (Se), spirulina (Spi), or selenium-enriched spirulina (SeSp). Sepsis was then induced by cecal ligature and puncture, and survival duration was observed. The plasma selenium concentration was measured by ICPMS. Expression of GPx1 and GPx3 mRNA was measured by RT-PCR. Blood parameters (lactates and HCO3- concentrations, pH, PO2 , and PCO2 ) were analyzed at 0, 1, and 2 h as well as inflammatory cytokines (IL-6, TNF-α, IL-10). Sodium selenite and SeSP supplementations restored plasma selenium concentration prior to sepsis. The survival duration of SeSP septic rats was significantly lower than that of selenium-supplemented ones. Gpx1 mRNA was increased after a selenium-enriched spirulina supplementation while Gpx3 mRNA levels remained unchanged. Furthermore, sodium selenite prevented sepsis-induced acidosis. Our results show that on a basis of a Se deficiency, selenium-enriched spirulina supplementations significantly worsen sepsis outcome when compared to Se supplementation. Furthermore, Se supplementation but not selenium-enriched spirulina supplementation decreased inflammation and restored acid-base equilibrium after a sepsis induction.

Carbon Dioxide Sensing-Biomedical Applications to Human Subjects.

Carbon dioxide (CO2) monitoring in human subjects is of crucial importance in medical practice. Transcutaneous monitors based on the Stow-Severinghaus electrode make a good alternative to the painful and risky arterial "blood gases" sampling. Yet, such monitors are not only expensive, but also bulky and continuously drifting, requiring frequent recalibrations by trained medical staff. Aiming at finding alternatives, the full panel of CO2 measurement techniques is thoroughly reviewed. The physicochemical working principle of each sensing technique is given, as well as some typical merit criteria, advantages, and drawbacks. An overview of the main CO2 monitoring methods and sites routinely used in clinical practice is also provided, revealing their constraints and specificities. The reviewed CO2 sensing techniques are then evaluated in view of the latter clinical constraints and transcutaneous sensing coupled to a dye-based fluorescence CO2 sensing seems to offer the best potential for the development of a future non-invasive clinical CO2 monitor.

Measuring hemoglobin spectra: searching for carbamino-hemoglobin.

SIGNIFICANCE: The arterial carbon dioxide (CO2) partial pressure PaCO2 is a clinically relevant variable. However, its measurement requires arterial blood sampling or bulky and expensive transcutaneous PtcCO2 meters. While the spectrophotometric determination of hemoglobin species-such as oxy-hemoglobin (O2Hb) and deoxy-hemoglobin (HHb)-allowed for the development of pulse oximetry, the measurement of CO2 blood content with minimal discomfort has not been addressed yet. AIM: Characterizing human carbamino-hemoglobin (CO2Hb) absorption spectrum, which is missing from the literature. Providing the theoretical background that will allow for transcutaneous, noninvasive PaCO2 measurements. APPROACH: A tonometry-based approach was used to obtain gas-equilibrated, lysed, diluted human blood. Equilibration was performed with both CO2, dinitrogen (N2), and ambient air. Spectrophotometric measurements were carried out on the 235- to 1000-nm range. A theoretical background was also derived from that of pulse oximetry. RESULTS: The absorption spectra of both CO2Hb and HHb were extremely close and comparable with that of state-of-the-art HHb. The above-mentioned theoretical background led to an estimated relative error above 30% on the measured amount of CO2Hb in a subject's blood. Auxiliary measurements revealed that the use of ethylene diamine tetraacetic acid did not interfere with spectrophotometric measurements, whereas sodium metabisulfite did. CONCLUSIONS: CO2Hb absorption spectrum was measured for the first time. Such spectrum being close to that of HHb, the use of a theoretical background based on pulse oximetry theory for noninvasive PaCO2 measurement seems extremely challenging.

Endothelial function may be enhanced in the cutaneous microcirculation after a single air dive.

INTRODUCTION: The effects of scuba diving on the vessel wall have been studied mainly at the level of large conduit arteries. Data regarding the microcirculation are scarce and indicate that these two vascular beds are affected differently by diving. METHODS: We assessed the changes in cutaneous microcirculation before an air scuba dive, then 30 min and 24 h after surfacing. Endothelium-dependent and independent vasomotion were successively elicited by iontophoretic administration of acetylcholine and sodium nitroprusside respectively, and cutaneous blood flux was monitored by laser Doppler flowmetry. RESULTS: The response to sodium nitroprusside was significantly lower 30 min after surfacing than before diving (50 (SEM 6)% of the pre-dive values, P = 0.0003) and returned to normal values 24 h post-dive (102 (29)% of the pre-dive values, P = 0.113). When compared to pre-dive values, acetylcholine elicited a hyperaemia which was not statistically different 30 min after surfacing (123 (17)% of the pre-dive values, P = 0.230), but significantly increased 24 h post-dive (148 (10)% of the pre-dive values, P = 0.005). CONCLUSION: Microvascular smooth muscle function is transiently impaired after diving. On the contrary, microvascular endothelial function is enhanced for up to 24 h after diving. This further suggests that the microcirculation reacts differently than large conduit arteries to scuba diving. The impact of modifications occurring in the microvascular bed on the physiological effects of diving merits further study.

Pre-hydration strongly reduces decompression sickness occurrence after a simulated dive in the rat.

INTRODUCTION: Hydration status is considered a parameter likely to influence the risk of decompression sickness (DCS), but scientific evidence is scarce and conflicting. This experiment aimed to analyse the influence of pre-hydration on DCS occurrence in a rat model. METHODS: Intra-peritoneal injections of saline solution were administered to rats (NaCl 0.9% 0 ml (Control), 0.1 ml (Group 1), or 1 ml·100g-1 body mass (Group 2) at each of 24 h, 12 h, and 30 min prior to simulated air dives (45 min at 1,010 kPa; compression and decompression rates 101 kPa·min-1; stops 5 min at 202 kPa, 5 min at 160 kPa, 10 min at 130 kPa). Evaluation of DCS occurrence and severity was made after decompression. RESULTS: Pre-dive hydration reduced severe DCS from 47% (Control) to 29% (Group 1) and 0% (Group 2), and increased the proportion of animals without any signs of DCS from 40 (Control) to 57% (Group 1) and 93% (Group 2); Chi2 P = 0.041. CONCLUSIONS: This experiment demonstrated that pre-hydration can drastically reduce the DCS occurrence in an animal model. In the context of scuba diving, this result highlights the importance of elucidating the mechanisms linking hydration status and DCS risk.

Combined effects of high hydrostatic pressure and dispersed oil on the metabolism and the mortality of turbot hepatocytes (Scophthalmus maximus).

Since the DeepWater Horizon oil spill and the use at 1450 m depth of dispersant as a technical response, the need of relevant ecotoxicological data on deep-sea ecosystems becomes crucial. In this context, this study focused on the effect of high hydrostatic pressure (10.1 MPa) on turbot hepatocytes isolated from fish exposed either to chemically dispersed oil, mechanically dispersed oil or dispersant alone. Potential combined effects of oil/dispersant and hydrostatic pressure, were assessed on cell mortality (total cell death, necrosis and apoptosis), cell viability and on hepatocyte oxygen consumption (MO2). No change in cell mortality was observed in any of the experimental conditions, whereas, the results of cell viability showed a strong and significant increase in the two oil groups independently of the pressure exposure. Finally, oil exposure and hydrostatic pressure have additive effects on oxygen consumption at a cellular level. Presence of dispersant prevent any MO2 increase in our experimental conditions. These mechanistic effects leading to this increased energetic demand and its eventual inhibition by dispersant must be investigated in further experiments.

Deep-sea versus shallow conditions: a comparative ecobarotoxicological study.

In the context of new oil exploration/production areas, knowledge of the biological impact of dispersed oil in the deep-sea environment is essential. Hence, the aim of this study was to perform a comparison, at atmospheric pressure (0.1 MPa) and at a high hydrostatic pressure corresponding to 1000 m depth (10.1 MPa), of lethal concentrations (LC) on a model fish, Scophthalmus maximus, exposed to chemically dispersed oil. Fish were exposed concomitantly at 0.1 and 10.1 MPa using two exposure tanks connected to the same source tank thanks to a closed circuit. Acute toxicity was evaluated at 24 h through the determination of LC10 and LC50 (respectively, 10 and 50% of mortality) calculated from measured total petroleum hydrocarbon concentrations in the water. No statistical differences were observed between the LC10 at 0.1 MPa (46.1 mg L- 1) and the LC10 at 10.1 MPa (31.0 mg L- 1), whereas the LC50 of fish exposed to 0.1 MPa (90.8 mg L- 1) was significantly higher than the LC50 at 10.1 MPa (50.9 mg L- 1). These results clearly show an increase in oil toxicity under high hydrostatic pressure. This effect may be due to synergistic effects of pressure and oil contamination on fish energetic metabolism.

Simulated air dives induce superoxide, nitric oxide, peroxynitrite, and Ca2+ alterations in endothelial cells.

Human diving is known to induce endothelial dysfunction. The aim of this study was to decipher the mechanism of ROS production during diving through the measure of mitochondrial calcium concentration, peroxynitrite, NO°, and superoxide towards better understanding of dive-induced endothelial dysfunction. Air diving simulation using bovine arterial endothelial cells (compression rate 101 kPa/min to 808 kPa, time at depth 45 min) was performed in a system allowing real-time fluorescent measurement. During compression, the cells showed increased mitochondrial superoxide, peroxynitrite, and mitochondrial calcium, and decreased NO° concentration. MnTBAP (peroxynitrite scavenger) suppressed superoxide, recovered NO° production and promoted stronger calcium influx. Superoxide and peroxynitrite were inhibited by L-NIO (eNOS inhibitor), but were further increased by spermine-NONOate (NO° donor). L-NIO induced stronger calcium influx than spermine-NONOate or simple diving. The superoxide and peroxynitrite were also inhibited by ruthenium red (blocker of mitochondrial Ca2+ uniporter), but were increased by CGP (an inhibitor of mitochondrial Na+-Ca2+ exchange). Reactive oxygen and nitrogen species changes are associated, together with calcium mitochondrial storage, with endothelial cell dysfunction during simulated diving. Peroxynitrite is involved in NO° loss, possibly through the attenuation of eNOS and by increasing superoxide which combines with NO° and forms more peroxynitrite. In the field of diving physiology, this study is the first to unveil a part of the cellular mechanisms of ROS production during diving and confirms that diving-induced loss of NO° is linked to superoxide and peroxynitrite.

New considerations on pathways involved in acute traumatic coagulopathy: the thrombin generation paradox.

Background: An acute traumatic coagulopathy (ATC) is observed in about one third of severely traumatized patients. This early, specific, and endogenous disorder is triggered by the association of trauma and hemorrhage. The early phase of this condition is characterized by the expression of a bleeding phenotype leading to hemorrhagic shock and the late phase by a prothrombotic profile leading to multiple organ failure. The physiopathology of this phenomenon is still poorly understood. Hypotheses of disseminated intravascular coagulation, activated protein C-mediated fibrinolysis, fibrinogen consumption, and platelet functional impairment were developed by previous authors and continue to be debated. The objective of this study was to observe general hemostasis disorders in case of ATC to confront these hypotheses. Method: Four groups of 15 rats were compared: C, control; T, trauma; H, hemorrhage; and TH, trauma and hemorrhage. Blood samples were drawn at baseline and 90 min. Thrombin generation tests, platelet aggregometry, and standard hemostasis tests were performed. Results: Significant differences were observed between the baseline and TH groups for aPTT (17.9 ± 0.8 s vs 24.3 ± 1.4 s, p < 0.001, mean ± SEM), MAP (79.7 ± 1.3 mmHg vs 43.8 ± 1.3 mmHg, p < 0.001, mean ± SEM), and hemoglobin (16.5 ± 0.1 g/dL vs 14.1 ± 0.3 g/dL, p < 0.001, mean ± SEM), indicating the presence of an hemorrhagic shock due to ATC. Compared to all other groups, coagulation factor activities were decreased in the TH group, but endogenous thrombin potential was (paradoxically) higher than in group C (312 ± 17 nM/min vs. 228 ± 23 nM/min; p = 0.016; mean ± SEM). We also observed a subtle decrease in platelet count and function in case of ATC and retrieved an inversed linear relationship between fibrinogen concentration and aPTT (intercept, 26.53 ± 3.16; coefficient, - 3.40 ± 1.26; adjusted R2: 0.1878; p = 0.0123). Conclusions: The clinical-biological profile that we observed, combining normal thrombin generation, fibrinogen depletion, and a hemorrhagic phenotype, reinforced the hypothesis of activated protein C mediated-fibrinolysis. The key role of fibrinogen, but not of the platelets, was confirmed in this study. The paradoxical preservation of thrombin generation suggests a protective mechanism mediated by rhabdomyolysis in case of major trauma. Based on these results, we propose a new conception concerning the pathophysiology of ATC.

A new form of admissible pressure for Haldanian decompression models.

In this article, we propose and study a new form of admissible pressure in the Haldanian framework. We then use it to study the surjectivity of the Gradient Factors on the space of the reachable decompression profiles, and investigate a particular case. This case leads to the proposition of a decompression strategy, whose crucial parameter is the ascent rate. An appropriate ascent rate is suggested as recommended by COMEX, through a physiologically relevantmethod. This new strategy enables the unification of the COMEX approach (not based on a tissuesaturation theory), with the Haldanian method.

Long-term atorvastatin treatment decreases heart maximal oxygen consumption and its vulnerability to in vitro oxidative stress in Watanabe heritable hyperlipidemic rabbit.

Statins are currently used in prevention of cardiovascular diseases in high-risk populations, and could be considered in primary prevention. However, few studies are available on the long-term effects of low doses of statins, especially on mitochondrial function and reactive oxygen species (ROS) metabolism at cardiac level. This study aimed to determine potential effects of a long-term atorvastatin treatment, at low-dose concentration, on the myocardium mitochondrial respiration. Thirty-four Watanabe rabbits were treated or not with atorvastatin (2.5 mg·kg-1·day-1) from the age of 3 to 12 months. Every 3 months, proton leak, basal (V0), and maximal (Vmax) mitochondrial respiration on cardiac permeabilized fibers were measured. Additionally, the vulnerability to ROS, cardiac enzymatic antioxidant defenses, and oxidative damage (lipoperoxidation) were analyzed. Proton leak increased over the duration of the experiment (up to 60% from Vmax at 12 months). Moreover, the statin treatment induced a decrease of Vmax and a decrease of ROS susceptibility of cardiac mitochondria. However, the lipoperoxidation and the antioxidant defenses were not dependent on the presence of statin treatment, or on its duration. This is the first study showing a protective effect of long-term statins treatment against the ROS susceptibility in the cardiac muscle.

Angiotensin Converting Enzyme Inhibitor Has a Protective Effect on Decompression Sickness in Rats.

Introduction: Commercial divers, high altitude pilots, and astronauts are exposed to some inherent risk of decompression sickness (DCS), though the mechanisms that trigger are still unclear. It has been previously showed that diving may induce increased levels of serum angiotensin converting enzyme. The renin angiotensin aldosterone system (RAAS) is one of the most important regulators of blood pressure and fluid volume. The purpose of the present study was to control the influence of angiotensin II on the appearance of DCS. Methods: Sprague Dawley rats have been pre-treated with inhibitor of angiotensin II receptor type 1 (losartan; 10 mg/kg), angiotensin-converting enzyme (ACE) inhibitor (enalapril; 10 mg/kg), and calcium-entry blocker (nifedipine; 20 mg/kg). The experimental groups were treated for 4 weeks before exposure to hyperbaric pressure while controls were not treated. Seventy-five rats were subjected to a simulated dive at 1000 kPa absolute pressure for 45 min before starting decompression. Clinical assessment took place over a period of 60 min after surfacing. Blood samples were collected for measurements of TBARS, interleukin 6 (IL-6), angiotensin II (ANG II) and ACE. Results: The diving protocol induced 60% DCS in non-treated animals. This ratio was significantly decreased after treatment with enalapril, but not other vasoactive drugs. Enalapril did not change ANG II or ACE concentration, while losartant decreased post dive level of ACE but not ANG II. None of the treatment modified the effect of diving on TBARS and IL-6 values. Conclusion: Results suggests that the rennin angiotensin system is involved in a process of triggering DCS but this has to be further investigated. However, a vasorelaxation mediated process, which potentially could increase the load of inert gas during hyperbaric exposure, and antioxidant properties were excluded by our results.

Venous gas emboli are involved in post-dive macro, but not microvascular dysfunction.

PURPOSE: Previous studies have shown vascular dysfunction of main conductance arteries and microvessels after diving. We aim to evaluate the impact of bubble formation on vascular function and haemostasis. To achieve this, we used a vibration preconditioning to influence bubble levels without changing any other parameters linked to the dive. METHODS: Twentty-six divers were randomly assigned to one of three groups: (1) the "vibrations-dive" group (VD; n = 9) was exposed to a whole-body vibration session 30 min prior the dive; (2) the "diving" group (D; n = 9) served as a control for the effect of the diving protocol; (3) The "vibration" protocol (V; n = 8) allowed us to assess the effect of vibrations without diving. Macro- and microvascular function was assessed for each subject before and after the dive, subsequently. Bubble grades were monitored with Doppler according to the Spencer grading system. Blood was taken before and after the protocol to assess any change of platelets or endothelial function. RESULTS: Bubble formation was lower in the VD than the diving group. The other measured parameters remained unchanged after the "vibration" protocol alone. Diving alone induced macrovascular dysfunction, and increased PMP and thrombin generation. Those parameters were no longer changed in the VD group. Conversely, a microvascular dysfunction persists despite a significant decrease of circulating bubbles. CONCLUSIONS: Finally, the results of this study suggest that macro- but not microvascular impairment results at least partly from bubbles, possibly related to platelet activation and generation of pro-coagulant microparticles.

Dispersed oil decreases the ability of a model fish (Dicentrarchus labrax) to cope with hydrostatic pressure.

Data on the biological impact of oil dispersion in deep-sea environment are scarce. Hence, the aim of this study was to evaluate the potential interest of a pressure challenge as a new experimental approach for the assessment of consequences of chemically dispersed oil, followed by a high hydrostatic pressure challenge. This work was conducted on a model fish: juvenile Dicentrarchus labrax. Seabass were exposed for 48 h to dispersant alone (nominal concentration (NC) = 4 mg L-1), mechanically dispersed oil (NC = 80 mg L-1), two chemically dispersed types of oil (NC = 50 and 80 mg L-1 with a dispersant/oil ratio of 1/20), or kept in clean seawater. Fish were then exposed for 30 min at a simulated depth of 1350 m, corresponding to pressure of 136 absolute atmospheres (ATA). The probability of fish exhibiting normal activity after the pressure challenge significantly increased from 0.40 to 0.55 when they were exposed to the dispersant but decreased to 0.26 and 0.11 in the case of chemical dispersion of oil (at 50 and 80 mg L-1, respectively). The chemical dispersion at 80 mg L-1 also induced an increase in probability of death after the pressure challenge (from 0.08 to 0.26). This study clearly demonstrates the ability of a pressure challenge test to give evidence of the effects of a contaminant on the capacity of fish to face hydrostatic pressure. It opens new perspectives on the analysis of the biological impact of chemical dispersion of oil at depth, especially on marine species performing vertical migrations.

A non-hypocholesterolemic atorvastatin treatment improves vessel elasticity by acting on elastin composition in WHHL rabbits.

BACKGROUND AND AIMS: Statins are prescribed for their preventative effects within atherosclerosis development. To our knowledge, no study focusing on very low-dose (non-hypolipidemic effect) and long-term atorvastatin treatment in vivo was available. Our aim was to assess the effect of such atorvastatin treatment on the mechanical and functional characteristics of arteries in the context of primary prevention. METHODS: An atorvastatin treatment (2.5 mg/kg/day) was tested against controls on 34 male 3 to 12 month-old WHHL rabbits. No effect on total cholesterol, triglycerides, HDL or LDL was observed. The arterial stiffness was evaluated on vigil animals by pulse wave velocity (PWV) measurement. Then, in vitro measurements were made to evaluate (1) the endothelial and vascular smooth muscle function, (2) the elasticity of the arterial wall and (3) the composition in collagen and elastin in the aorta. RESULTS: The PWV increasing observed with age in control group was canceled by treatment, creating a significance difference between groups at 12 months (5.17 ± 0.50 vs 2.14 ± 0.34 m s(-1) in control and treated groups respectively). Vasoreactivity modifications can't explain this result but maintain of elasticity with treatment in large arteries was confirm by a static tensile test. A first possible explanation is the change of wall composition with treatment, validated by the percentage of elastin at 12 months, 4.4% lower in the control group compared to the treated group (p < 0.05). CONCLUSIONS: This study shows that a non-hypocholesterolemic statin treatment could improve vessel elasticity in the atherosclerotic WHHL model. The great novelty of this work is the vessel wall composition changing associated. This first approach in animal opens the reflection on the use of these low doses in humans. This could be interesting in the context of arterial stiffening with aging, non-hyperlipidemic atherosclerosis or with cholesterol reduce by another therapy or lifestyle modification.

Effect of simulated air dive and decompression sickness on the plasma proteome of rats.

PURPOSE: Decompression sickness (DCS) is a poorly understood systemic disease caused by inadequate desaturation following a reduction in ambient pressure. Although recent studies highlight the importance of circulating factors, the available data are still puzzling. In this study, we aimed to identify proteins and biological pathways involved in the development of DCS in rats. EXPERIMENTAL DESIGN: Eighteen male Sprague-Dawley rats were subjected to a same simulated air dive to 1000 kPa absolute pressure and divided into two groups: no DCS or DCS. A third control group remained at atmospheric pressure. Venous blood was collected after hyperbaric exposure and the plasma proteomes from four individuals per group were analyzed by using a two-dimensional electrophoresis-based proteomic strategy. RESULTS: Quantitative analysis identified nine protein spots with abundances significantly changed (false discovery rate < 0.1) between the tested conditions. Three protein spots, identified as Apolipoprotein A1, Serine Protease Inhibitor A3K (Serpin A3K), and Alpha-1-antiproteinase, appeared increased in DCS animals but displayed only weak changes. By contrast, one protein spot identified as Transthyretin (TTR) dramatically decreased (i.e. quite disappeared) in animals displaying DCS symptoms. Before diving, TTR level was not different in DCS than nondiving group. CONCLUSION: These results may lead to the use of TTR as an early biomarker of DCS.

Influence of decompression sickness on vasocontraction of isolated rat vessels.

Studies conducted in divers indicate that endothelium function is impaired following a dive even without decompression sickness (DCS). Our previous experiment conducted on rat isolated vessels showed no differences in endothelium-dependent vasodilation after a simulated dive even in the presence of DCS, while contractile response to phenylephrine was progressively impaired with increased decompression stress. This study aimed to further investigate the effect of DCS on vascular smooth muscle. Thirty-two male Sprague-Dawley rats were submitted to the same hyperbaric protocol and classified according to the severity of DCS: no-DCS (without clinical symptoms), mild-DCS, or severe-DCS (dead within 1 h). A control group remained at atmospheric pressure. Isometric tension was measured in rings of abdominal aorta and mesenteric arteries. Single dose contraction was assessed with KCl solution. Dose-response curves were obtained with phenylephrine and endothelin-1. Phenylephrine-induced contraction was observed in the presence of antioxidant tempol. Additionally, plasma concentrations of angiotensin II, angiotensin-converting enzyme, and thiobarbituric acid reactive substances (TBARS) were assessed. Response to phenylephrine was impaired only among mild-DCS in both vessels. Dose-response curves to endothelin-1 were impaired after mild-DCS in mesenteric and severe-DCS in aorta. KCl-induced contraction was affected after hyperbaric exposure regardless of DCS status in aorta only. These results confirm postdive vascular dysfunction is dependent on the type of vessel. It further evidenced that vascular dysfunction is triggered by DCS rather than by diving itself and suggest the influence of circulating factor/s. Diving-induced impairment of the L-type voltage-dependent Ca(2+) channels and/or influence of renin-angiotensin system is proposed.

Age, weight and decompression sickness in rats.

OBJECTIVE: The aim of this study was to determine if, after controlling for weight, age is associated with decompression sickness (DCS) in rats. METHODS: Following compression-decompression, male rats aged 11 weeks were observed for DCS. After two weeks recovery, surviving rats were re-dived using the same compression-decompression profile. RESULTS: In this experiment, there was a clear difference between DCS outcome at ages 11 or 13 weeks in matched rats (p = 0.002). DISCUSSION: Even with weight included in the model, age was significantly associated with DCS (p = 0.01), yet after removal of weight the association was much stronger (p = 0.002). CONCLUSION: We believe that age is likely to be found associated with the probability of DCS in a larger dataset with a wider range of parameters, after accounting for the effect of weight.