Platelet activation in rabbits with decompression sickness.

Platelets are the most easily altered type of peripheral blood cell in decompression sickness (DCS), which can feature decreased platelet count and the appearance of platelet microparticles in plasma. We hypothesized that DCS results in platelet activation in the bloodstream. The present study was carried out on 45 rabbits. The platelet count and concentration of plasma platelet markers were determined in 35 rabbits; the platelet shape was observed under scanning electron microscope in 10 rabbits. All indexes were collected at two points: 24 hours before the simulated dive and 30 minutes after the simulated dive. Platelet count decreased noticeably after DCS, from 380.10 ± 73.61 (G/L) to 330.23 ± 115.72 (G/L), a change of approximately -13.49 ± 25.57 (%). Platelet count was further decreased in the severe DCS group (a change of -45.99 ± 18.57%). Platelet count after DCS was proportional to the survival time of the rabbits after DCS. The concentration of two plasma platelet markers (PF4 and BTG) did not demonstrate statistically significant change at 30 minutes after DCS. However, platelet shape was changed, and the following features were observed: oblong, distortion, flattening shape, sticking together, mixing of membrane, and abundance of pseudopods with a 100- to 200-nm diameter. We conclude there is platelet activation in the bloodstream in cases of DCS.

COVID-19-related complications and decompression illness share main features.: Could the SARS-CoV2-related complications rely on blood foaming?

A study by Saraiva et al. (2011) demonstrated the presence of Angiotensin II receptors on the erythrocyte membrane. This little-known information should be deemed as crucial as the SARS-CoV-2 relationships with oxygen saturation and the Renine Angiotensin System but it currently remains unexploited. The pulmonary and cardiovascular systems are involved in any typical complications of COVID-19 but numerous other unrelated symptoms may occur. To fill the gap, we shall first emphasize some similarities between the complications of this infectious disease and Decompression Illness (DCI), which involves bubble formation. We theorized that the Angiotensin II clearance by the red blood cells could trigger the release of its oxygen content in the bloodstream. The resulting foam would worsen the widespread endotheliitis, worsen the gas exchange, trigger the coagulation process, the inflammation process and the complement pathway as typically occurs in DCI. At the end, we propose a plausible mechanism.

An explicitly multi-component arterial gas embolus dissolves much more slowly than its one-component approximation.

We worked out the growth and dissolution rates of an arterial gas embolism (AGE), to illustrate the evolution over time of its size and composition, and the time required for its total dissolution. We did this for a variety of breathing gases including air, pure oxygen, Nitrox and Heliox (each over a range of oxygen mole fractions), in order to assess how the breathing gas influenced the evolution of the AGE. The calculations were done by numerically integrating the underlying rate equations for explicitly multi-component AGEs, that contained a minimum of three (water, carbon dioxide and oxygen) and a maximum of five components (water, carbon dioxide, oxygen, nitrogen and helium). The rate equations were straight-forward extensions of those for a one-component gas bubble. They were derived by using the Young-Laplace equation and Dalton's law for the pressure in the AGE, the Laplace equation for the dissolved solute concentration gradients in solution, Henry's law for gas solubilities, and Fick's law for diffusion rates across the AGE/arterial blood interface. We found that the 1-component approximation, under which the contents of the AGE are approximated by its dominant component, greatly overestimates the dissolution rate and underestimates the total dissolution time of an AGE. This is because the 1-component approximation manifestly precludes equilibration between the AGE and arterial blood of the inspired volatile solutes (O2, N2, He) in arterial blood. Our calculations uncovered an important practical result, namely that the administration of Heliox, as an adjunct to recompression therapy for treating a suspected N2-rich AGE must be done with care. While Helium is useful for preventing nitrogen narcosis which can arise in aggressive recompression therapy wherein the N2 partial pressure can be quite high (e.g.∼5 atm), it also temporarily expands the AGE, beyond the expansion arising from the use of Oxygen-rich Nitrox. For less aggressive recompression therapy wherein nitrogen narcosis is not a significant concern, Oxygen-rich Nitrox is to be preferred, both because it does not temporarily expand the AGE as much as Heliox, and because it is much cheaper and more conservation-minded.

In vitro evidence of decompression bubble dynamics and gas exchange on the luminal aspect of blood vessels: Implications for size distribution of venous bubbles.

We found that lung surfactant leaks into the bloodstream, settling on the luminal aspect of blood vessels to create active hydrophobic spots (AHS). Nanobubbles formed by dissolved gas at these AHS are most probably the precursors of gas micronuclei and decompression bubbles. Sheep blood vessels stretched on microscope slides, and exposed under saline to hyperbaric pressure, were photographed following decompression. Photographs of an AHS from a pulmonary vein, containing large numbers of bubbles, were selected in 1-min sequences over a period of 7 min, starting 18 min after decompression from 1,013 kPa. This showed bubble detachment, coalescence and expansion, as well as competition for dissolved gas between bubbles. There was greater expansion of peripheral than of central bubbles. We suggest that the dynamics of decompression bubbles on the surface of the blood vessel may be the closest approximation to true decompression physiology, and as such can be used to assess and calibrate models of decompression bubbles. We further discuss the implications for bubble size in the venous circulation.

Elevated Environmental Carbon Dioxide Exposure Confounding Physiologic Events in Aviators?

INTRODUCTION: Physiological events (PEs) are a growing problem for US military aviation with detrimental risks to safety and mission readiness. Seeking causative factors is, therefore, of high importance. There is no evidence to date associating carbon dioxide (CO2) pre-flight exposure and decompression sickness (DCS) in aviators. MATERIALS AND METHODS: This study is a case series of six aviators with PE after being exposed to a rapid decompression event (RDE) with symptoms consistent with type II DCS. The analysis includes retrospective review of flight and environmental data to further assess a possible link between CO2 levels and altitude physiologic events (PEs). IRB approval was obtained for this study. RESULTS: This case series presents six aviators with PE after being exposed to a rapid decompression event (RDE) with symptoms consistent with type II DCS. Another three aviators were also exposed to a RDE, but remained asymptomatic. All events involved tactical jet aircraft flying at an average of 35,600' Mean Sea Level (MSL) when a RDE occurred, Retrospective reviews led to the discovery that the affected individuals were exposed, pre-flight, to poor indoor air quality demonstrated by elevated levels of measured CO2. CONCLUSION: PEs are a growing safety concern for the aviation community in the military. As such, increasing measures are taken to ensure safety of flight and completion of the mission. To date, there is no correlation of CO2 exposure and altitude DCS. While elevated CO2 levels cannot be conclusively implicated as causative, this case series suggests a potential role of CO2 in altitude DCS through CO2 direct involvement with emboli gas composition, as well as pro-inflammatory cascade. Aviators exposed to elevated CO2 in poorly ventilated rooms developed PE symptoms consistent with DCS, while at the same command, aviators that were exposed to a well ventilated room did not. This report is far from an answer, but does demonstrate an interesting case series that draws some questions about CO2's role in these aviator's DCS experience. Other explanations are plausible, including the accurate diagnosis of DCS, health variables amongst the aviators, and differences in aircraft and On-Board Oxygen Generation Systems (OBOGS). For a better understanding, the role of environmental CO2 and pre-flight exposure as a risk of DCS should be reviewed.

Nitrogen Washout and Venous Gas Emboli During Sustained vs. Discontinuous High-Altitude Exposures.

INTRODUCTION: The frequency of long-duration, high-altitude missions with fighter aircraft is increasing, which may increase the incidence of decompression sickness (DCS). The aim of the present study was to compare decompression stress during simulated sustained high-altitude flying vs. high-altitude flying interrupted by periods of moderate or marked cabin pressure increase.METHODS: The level of venous gas emboli (VGE) was assessed from cardiac ultrasound images using the 5-degree Eftedal-Brubakk scale. Nitrogen washout/uptake was measured using a closed-circuit rebreather. Eight men were investigated in three conditions: one 80-min continuous exposure to a simulated cabin altitude of A) 24,000 ft, or four 20-min exposures to 24,000 ft interspersed by three 20-min intervals at B) 20,000 ft or C) 900 ft.RESULTS: A and B induced marked and persistent VGE, with peak bubble scores of [median (range)]: A: 2.5 (1-3); B: 3.5 (2-4). Peak VGE score was less in C [1.0 (1-2), P < 0.01]. Condition A exhibited an initially high and exponentially decaying rate of nitrogen washout. In C the washout rate was similar in each period at 24,000 ft, and the nitrogen uptake rate was similar during each 900-ft exposure. B exhibited nitrogen washout during each period at 24,000 ft and the initial period at 20,000 ft, but on average no washout or uptake during the last period at 20,000 ft.DISCUSSION: Intermittent reductions of cabin altitude from 24,000 to 20,000 ft do not appear to alleviate the DCS risk, presumably because the pressure increase is not sufficient to eliminate VGE. The nitrogen washout/uptake rate did not reflect DCS risk in the present exposures.Ånell R, Grönkvist M, Eiken O, Gennser M. Nitrogen washout and venous gas emboli during sustained vs. discontinuous high-altitude exposures. Aerosp Med Hum Perform. 2019; 90(6):524-530.

Ovine plasma dipalmitoylphosphatidylcholine does not predict decompression bubbling.

Decompression illness (DCI) is the main risk associated with scuba diving. Some divers ("bubblers") are more sensitive to DCI than others ("non-bubblers"). We found that there are active hydrophobic spots (AHS) on the luminal aspect of ovine blood vessels, which contain the surfactant dipalmitoylphosphatidylcholine (DPPC). DPPC leaks from the lung into the plasma, settling on the blood vessel to create AHS. These are the main source of gas micronuclei from which bubbles develop after decompression. A correlation between bubbling ovine blood vessels and the animal's plasma DPPC might lead to the development of a blood test for vulnerability to DCI. Samples from ovine blood vessels were stretched on microscope slides, placed anaerobically in saline at the bottom of a Pyrex bowl, and exposed to high pressure. Automated photography was used after decompression to reveal AHS by visualising their bubble production. Phospholipids were extracted from the AHS and plasma for determination of DPPC. Bubbling was unrelated to the concentration of DPPC in the plasma (2.15 ±â€¯0.87 µg/ml). Bubble production from the AHS (n = 130) as a function of their DPPC content yielded two groups, one unrelated to DPPC and the other which demonstrated increased bubbling with elevation of DPPC. We suggest this may be related to alternate layering with hydrophobic and hydrophilic phospholipids. This study reinforces the connection between DPPC and DCI. However, a blood test for diver vulnerability to decompression stress is not recommended.

Benefits of hyperbaric oxygen pretreatment for decompression sickness in Bama pigs.

Decompression sickness (DCS) occurs when ambient pressure is severely reduced during diving and aviation. Hyperbaric oxygen (HBO) pretreatment has been shown to exert beneficial effects on DCS in rats via heat-shock proteins (HSPs). We hypothesized that HBO pretreatment will also reduce DCS via HSPs in swine models. In the first part of our investigation, six swine were subjected to a session of HBO treatment. HSP32, 60, 70 and 90 were detected, before and at 6, 12, 18, 24 and 30 h following exposure in lymphocytes. In the second part of our investigation, another 10 swine were randomly assigned into two groups (five per group). All swine were subjected to two simulated air dives in a hyperbaric chamber with an interval of 7 days. Eighteen hours before each dive, the swine were pretreated with HBO or air: the first group received air pretreatment prior to the first dive and HBO pretreatment prior to the second; the second group were pretreated with HBO first and then air. Bubble loads, skin lesions, inflammation and endothelial markers were detected after each dive. In lymphocytes, all HSPs increased significantly (P<0.05), with the greatest expression appearing at 18 h for HSP32 and 70. HBO pretreatment significantly reduced all the determined changes compared with air pretreatment. The results demonstrate that a single exposure to HBO 18 h prior to diving effectively protects against DCS in the swine model, possibly via induction of HSPs.

Metabonomic potential plasma biomarkers in abnormal fast buoyancy ascent escape-induced decompression sickness model and the protective effects of pyrrolidine dithiocarbamic acid.

BACKGROUND: Decompression sickness (DCS) induced by fast buoyancy ascent escape (FBAE) is a special DCS, characterized with cardiopulmonary injuries. Serum metabonomics of this type of DCS has not yet been studied. We proposed a metabonomics approach for assessing serum metabonomics changes and evaluating the preventive effect of pyrrolidine dithiocarbamic acid (PDTC) in FBAE-induced DCS rats. METHODS: Sixty-five (65) rats were divided into three groups, including the Control, DCS and PDTC groups. After receiving physiological saline or PDTC pretreatment, rats in the DCS and PDTC groups received the same protocol of simulated FBAE. Following this, a metabonomics approach - combined with pattern recognition methods including PCA and PLS-DA - was used to characterize the global serum metabolic profile on survival rats (five rats per group) associated with abnormal FBAE-induced DCS. As the VIP-value threshold cutoff of the metabolites was set to 2, metabolites above this threshold were filtered out as potential target biomarkers. RESULTS: Sixteen (16) distinct potential biomarkers in rat plasma were identified. PDTC significantly lowered DSC mortality from 60% to 10%, and alleviated ultrastructural alteration of the left ventricular apex compared to the DCS group. It was found that abnormal FBAE-induced DCS was closely related to disturbed fatty acid metabolism, glycerophospholipid metabolism, sterol lipid metabolism, and bile acid metabolism. With the presented metabonomic method, we systematically analyzed the protective effects of PDTC. CONCLUSION: The results demonstrated that PDTC administration could provide satisfactory effects on abnormal FBAE-induced DCS through partially regulating the perturbed metabolic pathways.

Probabilistic pharmacokinetic models of decompression sickness in humans, part 1: Coupled perfusion-limited compartments.

Decompression sickness (DCS) is a disease caused by gas bubbles forming in body tissues following a reduction in ambient pressure, such as occurs in scuba diving. Probabilistic models for quantifying the risk of DCS are typically composed of a collection of independent, perfusion-limited theoretical tissue compartments which describe gas content or bubble volume within these compartments. It has been previously shown that 'pharmacokinetic' gas content models, with compartments coupled in series, show promise as predictors of the incidence of DCS. The mechanism of coupling can be through perfusion or diffusion. This work examines the application of five novel pharmacokinetic structures with compartments coupled by perfusion to the prediction of the probability and time of onset of DCS in humans. We optimize these models against a training set of human dive trial data consisting of 4335 exposures with 223 DCS cases. Further, we examine the extrapolation quality of the models on an additional set of human dive trial data consisting of 3140 exposures with 147 DCS cases. We find that pharmacokinetic models describe the incidence of DCS for single air bounce dives better than a single-compartment, perfusion-limited model. We further find the U.S. Navy LEM-NMRI98 is a better predictor of DCS risk for the entire training set than any of our pharmacokinetic models. However, one of the pharmacokinetic models we consider, the CS2T3 model, is a better predictor of DCS risk for single air bounce dives and oxygen decompression dives. Additionally, we find that LEM-NMRI98 outperforms CS2T3 on the extrapolation data.

Evolution of the plasma proteome of divers before and after a single SCUBA dive.

PURPOSE: Decompression sickness (DCS) is a poorly understood and complex systemic disease caused by inadequate desaturation following a reduction of ambient pressure. A previous proteomic study of ours showed that DCS occurrence but not diving was associated with changes in the plasma proteome in rats, including a dramatic decrease of abundance of the tetrameric form of Transthyretin (TTR). The present study aims to assess the impact on the human blood proteome of a dive inducing significant decompression stress but without inducing DCS symptoms. EXPERIMENTAL DESIGN: Twelve healthy male divers were subjected to a single dive at a depth of 18 m of sea water (msw) with a 47-min bottom time followed by a direct ascent to the surface at a rate of 9 msw/min. Venous blood was collected before the dive as well as 30 min and 2 h following the dive. The plasma proteomes from four individuals were then analyzed by using a two-dimensional electrophoresis-based proteomic strategy. RESULTS: No protein spot showed a significantly changed abundance (fdr< 0.1) between the tested times. CONCLUSION: These results strengthen the hypothesis according to which significant changes of the plasma proteome measurable with two-dimensional electrophoresis may only occur along with DCS symptoms.

Decompression illness with hypovolemic shock and neurological failure symptoms after two risky dives: a case report.

Hypovolemia is known to be a predisposing factor of decompression illness (DCI) while diving. The typical clinically impressive neurological symptoms of DCI may distract from other symptoms such as an incipient hypovolemic shock. We report the case of a 61-year-old male Caucasian, who presented with an increasing central and peripheral neural failure syndrome and massive hypovolemia after two risky dives. Computed tomography (CT) scans of the chest and Magnetic resonance imaging scans of the head revealed multiple cerebral and pulmonary thromboembolisms. Transesophageal echocardiography showed a patent foramen ovale (PFO). Furthermore, the patient displayed hypotension as well as prerenal acute kidney injury with elevated levels of creatinine and reduced renal clearance, indicating a hypovolemic shock. Early hyperbaric oxygen (HBO) therapy reduced the neurological deficits. After volume expansion of 11 liters of electrolyte solution (1000 mL/h) the cardiopulmonary and renal function normalized. Hypovolemia increases the risk of DCI during diving and that of hypovolemic shock. Early HBO therapy and fluid replacement is crucial for a favorable outcome.

Preventive effect of rosiglitazone on liver injury in a mouse model of decompression sickness.

BACKGROUND AND AIMS: Severe decompression sickness (DCS) is a multi-organ injury. This study investigated the preventive effects of rosiglitazone on liver injury following rapid decompression in mice and examined the underlying mechanisms. METHODS: Mice were randomly divided into four groups: a control group, vehicle group, and rosiglitazone (5 and 10 mg·kg⁻¹) groups, the latter three being exposed to a pressure of 911 kPa. Haematoxylin and eosin staining, plasma levels of alanine transaminase (ALT), aspartate transaminase (AST) and lactate dehydrogenase and blood cell counts were used to evaluate liver injury at 30 min after rapid decompression. The expression of endothelial and inducible nitric oxide synthase (iNOS) and its phosphorylation were measured to uncover the underlying molecular mechanisms. RESULTS: A significant increase in plasma ALT, red blood cells and platelets, and a decrease in neutrophils were observed in the vehicle group. Furthermore, the expression of iNOS, E-selectin and the total level of NO in hepatic tissue, and soluble E-selectin in the plasma were significantly elevated in the vehicle group. Rosiglitazone pre-treatment prevented the increases in ALT (and AST), soluble E-selectin concentration, red blood cells and platelet counts. Moreover, rosiglitazone reduced over-expression of iNOS and the NO level, prevented the fall in neutrophil count and promoted the phosphorylation of iNOS in the liver. CONCLUSIONS: Pre-treatment with rosiglitazone ameliorated liver injury from severe DCS. This preventive effect may be partly mediated by stimulating endothelial NO production, improving endothelial function and limiting inflammatory processes.

Endothelia-Targeting Protection by Escin in Decompression Sickness Rats.

Endothelial dysfunction is involved in the pathogenesis of decompression sickness (DCS) and contributes substantively to subsequent inflammatory responses. Escin, the main active compound in horse chestnut seed extract, is well known for its endothelial protection and anti-inflammatory properties. This study aimed to investigate the potential protection of escin against DCS in rats. Escin was administered orally to adult male rats for 7 d (1.8 mg/kg/day) before a simulated air dive. After decompression, signs of DCS were monitored, and blood and pulmonary tissue were sampled for the detection of endothelia related indices. The incidence and mortality of DCS were postponed and decreased significantly in rats treated with escin compared with those treated with saline (P < 0.05). Escin significantly ameliorated endothelial dysfunction (increased serum E-selectin and ICAM-1 and lung Wet/Dry ratio, decreased serum NO), and oxidative and inflammatory responses (increased serum MDA, MPO, IL-6 and TNF-α) (P < 0.05 or P < 0.01). The results suggest escin has beneficial effects on DCS related to its endothelia-protective properties and might be a drug candidate for DCS prevention and treatment.

Endothelial dysfunction correlates with decompression bubbles in rats.

Previous studies have documented that decompression led to endothelial dysfunction with controversial results. This study aimed to clarify the relationship between endothelial dysfunction, bubble formation and decompression rate. Rats were subjected to simulated air dives with one of four decompression rates: one slow and three rapid. Bubble formation was detected ultrasonically following decompression for two hours, before measurement of endothelial related indices. Bubbles were found in only rapid-decompressed rats and the amount correlated with decompression rate with significant variability. Serum levels of ET-1, 6-keto-PGF1α, ICAM-1, VCAM-1 and MDA, lung Wet/Dry weight ratio and histological score increased, serum NO decreased following rapid decompression. Endothelial-dependent vasodilatation to Ach was reduced in pulmonary artery rings among rapid-decompressed rats. Near all the above changes correlated significantly with bubble amounts. The results suggest that bubbles may be the causative agent of decompression-induced endothelial damage and bubble amount is of clinical significance in assessing decompression stress. Furthermore, serum levels of ET-1 and MDA may serve as sensitive biomarkers with the capacity to indicate endothelial dysfunction and decompression stress following dives.

Pathophysiological and diagnostic implications of cardiac biomarkers and antidiuretic hormone release in distinguishing immersion pulmonary edema from decompression sickness.

Immersion pulmonary edema (IPE) is a misdiagnosed environmental illness caused by water immersion, cold, and exertion. IPE occurs typically during SCUBA diving, snorkeling, and swimming. IPE is sometimes associated with myocardial injury and/or loss of consciousness in water, which may be fatal. IPE is thought to involve hemodynamic and cardiovascular disturbances, but its pathophysiology remains largely unclear, which makes IPE prevention difficult. This observational study aimed to document IPE pathogenesis and improve diagnostic reliability, including distinguishing in some conditions IPE from decompression sickness (DCS), another diving-related disorder.Thirty-one patients (19 IPE, 12 DCS) treated at the Hyperbaric Medicine Department (Ste-Anne hospital, Toulon, France; July 2013-June 2014) were recruited into the study. Ten healthy divers were recruited as controls. We tested: (i) copeptin, a surrogate marker for antidiuretic hormone and a stress marker; (ii) ischemia-modified albumin, an ischemia/hypoxia marker; (iii) brain-natriuretic peptide (BNP), a marker of heart failure, and (iv) ultrasensitive-cardiac troponin-I (cTnI), a marker of myocardial ischemia.We found that copeptin and cardiac biomarkers were higher in IPE versus DCS and controls: (i) copeptin: 68% of IPE patients had a high level versus 25% of DCS patients (P < 0.05) (mean ±â€Šstandard-deviation: IPE: 53 ±â€Š61 pmol/L; DCS: 15 ±â€Š17; controls: 6 ±â€Š3; IPE versus DCS or controls: P < 0.05); (ii) ischemia-modified albumin: 68% of IPE patients had a high level versus 16% of DCS patients (P < 0.05) (IPE: 123 ±â€Š25 arbitrary-units; DCS: 84 ±â€Š25; controls: 94 ±â€Š7; IPE versus DCS or controls: P < 0.05); (iii) BNP: 53% of IPE patients had a high level, DCS patients having normal values (P < 0.05) (IPE: 383 ±â€Š394 ng/L; DCS: 37 ±â€Š28; controls: 19 ±â€Š15; IPE versus DCS or controls: P < 0.01); (iv) cTnI: 63% of IPE patients had a high level, DCS patients having normal values (P < 0.05) (IPE: 0.66 ±â€Š1.50 µg/L; DCS: 0.0061 ±â€Š0.0040; controls: 0.0090 ±â€Š0.01; IPE versus DCS or controls: P < 0.01). The combined "BNP-cTnI" levels provided most discrimination: all IPE patients, but none of the DCS patients, had elevated levels of either/both of these markers.We propose that antidiuretic hormone acts together with a myocardial ischemic process to promote IPE. Thus, monitoring of antidiuretic hormone and cardiac biomarkers can help to make a quick and reliable diagnosis of IPE.

Diving into the rat plasma proteome to get to the bottom of decompression sickness.

Decompression sickness (DCS) is the collective term for an array of signs and symptoms triggered by ambient pressure reduction. It is of particular concern to divers as they decompress on ascend from depth to sea surface, but despite a long history of studies the determinants of DCS risk are incompletely understood and there are no validated biomarkers. In this issue of Proteomics Clinical Applications, Lautridou et al. [8] report on their search for DCS biomarkers in rats exposed to simulated diving. By comparing the plasma proteomes from animals showing neurological symptoms to those emerging from dives unaffected, they identified several high-abundance proteins not previously associated with DCS. The most significant finding was a near depletion of thyroxine- and vitamin A transporter transthyretin in symptomatic rats. In addition to their potential role as diagnostic biomarkers, the proteins identified in Lautridou's study may offer new pieces in the yet incomplete puzzle of DCS etiology.

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.

Effects of Hyperbaric and Decompression Stress on Blood Coagulation and Fibrinolysis: Comparison of Thromboelastography and Thromboelastometry.

Hyperbaric and decompression stress from diving impairs blood coagulation and fibrinolysis. We hypothesized that thromboelastography (TEG) and rotational thromboelastometry (ROTEM) were suitable to characterize the effects of stress on global hemostatic profiles. We thus conducted a comparative study of the hyperbaric effects on human coagulation using TEG and ROTEM. Maximum clot strength (maximum amplitude [MA]) and clot lysis (lysis index at time 30 minutes [LI30]) were reduced as indicated by TEG MA and EXTEM LI30, respectively. The relative changes in coagulation and fibrinolysis by the hyperbaric effects of diving were indicated by reduced TEG reaction time R at 5 hours, MA at 24 hours postdive, and reduced EXTEM coagulation time at 15 minutes postdive as well as decreased fibrinolysis (EXTEM LI30) at all postdiving time points investigated. Comparison of the parameter values and the diving-induced changes in each parameter between TEG and ROTEM showed both differences and correlations. The discrepancies between the 2 systems may be due to the different assay reagents used. Future studies will seek to further elucidate the changes in blood coagulation and fibrinolysis following varying levels of hyperbaric and decompression stress.