Effects of successive air and nitrox dives on human vascular function

SCUBA diving is regularly associated with asymptomatic changes in cardiac, pulmonary and vascular function. The aim of this study was to evaluate the changes in vascular/endothelial function following SCUBA diving and to assess the potential difference between two breathing gases: air and nitrox 36 (36% oxygen and 64% nitrogen). Ten divers performed two 3-day diving series (no-decompression dive to 18 m with 47 min bottom time with air and nitrox, respectively), with 2 weeks pause in between. Arterial/endothelial function was assessed using SphygmoCor and flow-mediated dilation measurements, and concentration of nitrite before and after diving was determined in venous blood. Production of nitrogen bubbles post-dive was assessed by ultrasonic determination of venous gas bubble grade. Significantly higher bubbling was found after all air dives as compared to nitrox dives. Pulse wave velocity increased slightly (~6%), significantly after both air and nitrox diving, indicating an increase in arterial stiffness. However, augmentation index became significantly more negative after diving indicating smaller wave reflection. There was a trend for post-dive reduction of FMD after air dives; however, only nitrox diving significantly reduced FMD. No significant differences in blood nitrite before and after the dives were found. We found that nitrox diving affects systemic/vascular function more profoundly than air diving by reducing FMD response, most likely due to higher oxygen load. Both air and nitrox dives increased arterial stiffness, but decreased wave reflection suggesting a decrease in peripheral resistance due to exercise during diving. These effects of nitrox and air diving were not followed by changes in plasma nitrite.     

Computer validation and statistical correlations of a modern decompression diving algorithm

A diving algorithm is a safe combination of model and data to efficiently stage diver ascents following arbitrary underwater exposures. To that end, we detail a modern one, the LANL reduced gradient bubble model (RGBM), dynamical principles, and correlations with the LANL Data Bank data. Table, profile, and meter fit and risk parameters are obtained in statistical likelihood analysis from decompression exposure data. The RGBM algorithm enjoys extensive and utilitarian application in mixed gas diving, both in recreational and technical sectors, and forms the bases for released tables, software, and decompression meters used by scientific, commercial, and research divers. The LANL Data Bank is described, and the methods used to deduce risk are detailed. Risk functions for dissolved gas and bubbles are summarized. Parameters that can be used to estimate profile risk are tallied. To fit data, a modified Levenberg-Marquardt routine is employed. The LANL Data Bank presently contains 2879 profiles with 20 cases of DCS across nitrox, trimix, and heliox deep and decompression diving. This work establishes needed correlation between global mixed gas diving, specific bubble model, and deep stop data. Our objective is operational diving, not clinical science. The fit of bubble model to deep stop data is chi squared significant to 93%, using the logarithmic likelihood ratio of null set (actual set) to fit set. The RGBM algorithm is thus validated within the LANL Data Bank. Extensive and safe utilization of the model reported in field user statistics for tables, meters, and software also suggests real world validation, that is, one without noted nor reported DCS spikes in the field.     

Degassed liquids to prevent/treat decompression sickness

Recompression and oxygen breathing constitute the primary treatments for decompression sickness (DCS). Increasing the volume of distribution of dissolved gas with high-volume liquid therapy represents an alternative strategy to prevent or treat DCS. Furthermore, degassing of ingested and infused liquids would increase their potential to keep supersaturated tissue gases in solution after decompression. We hypothesize that administration of degassed liquids will prevent or reverse mild-moderate DCS by increasing the volume of distribution of dissolved gas in DCS victims. Degassed perfluorocarbon ingestion offers particularly attractive potential: one liter theoretically dissolves approximately 300ml of N(2) in vivo at 1atm. One could speculate that degassed liquids may adequately treat mild DCS in lieu of recompression, particularly DCS expressed in 'fast compartment' (well-perfused) tissues. Furthermore, degassed liquid administration should prove to be even more effective adjunct therapy for severe DCS than present gas-saturated liquids.     

Use of heart rate monitoring for an individualized and time-variant decompression model

Individual differences, physiological pre-conditions and in-dive conditions like workload and body temperature have been known to influence bubble formation and risk of decompression sickness in diving. Despite this fact, such effects are currently omitted from the decompression algorithms and tables that are aiding the divers. There is an apparent need to expand the modeling beyond depth and time to increase safety and efficiency of diving. The present paper outlines a mathematical model for how heart rate monitoring in combination with individual parameters can be used to obtain a customized and time-variant decompression model. We suggest that this can cover some of the individual differences and dive conditions that are affecting bubble formation. The model is demonstrated in combination with the previously published Copernicus decompression model, and is suitable for implementation in dive computers and post dive simulation software for more accurate risk analysis.     

Effect of in-water recompression with oxygen to 6 msw versus normobaric oxygen breathing on bubble formation in divers

It is generally accepted that the incidence of decompression sickness (DCS) from hyperbaric exposures is low when few or no bubbles are present in the circulation. To date, no data are available on the influence of in-water oxygen breathing on bubble formation following a provocative dive in man. The purpose of this study was to compare the effect of post-dive hyperbaric versus normobaric oxygen breathing (NOB) on venous circulating bubbles. Nineteen divers carried out open-sea field air dives at 30 msw depth for 30 min followed by a 9 min stop at 3 msw. Each diver performed three dives: one control dive, and two dives followed by 30 min of hyperbaric oxygen breathing (HOB) or NOB; both HOB and NOB started 10 min after surfacing. For HOB, divers were recompressed in-water to 6 msw at rest, whereas NOB was performed in a dry room in supine position. Decompression bubbles were examined by a precordial pulsed Doppler. Bubble count was significantly lower for post-dive NOB than for control dives. HOB dramatically suppressed circulating bubble formation with a bubble count significantly lower than for NOB or controls. In-water recompression with oxygen to 6 msw is more effective in removing gas bubbles than NOB. This treatment could be used in situations of “interrupted” or “omitted” decompression, where a diver returns to the water in order to complete decompression prior to the onset of symptoms. Further investigations are needed before to recommend this protocol as an emergency treatment for DCS.     

Treatment of micro air bubbles in rat adipose tissue at 25 kPa altitude exposures with perfluorocarbon emulsions and nitric oxide

Introduction

Perfluorocarbon emulsions (PFC) and nitric oxide (NO) releasing agents have on experimental basis demonstrated therapeutic properties in treating and preventing the formation of venous gas embolism as well as increased survival rate during decompression sickness from diving. The effect is ascribed to an increased solubility and transport capacity of respiratory gases in the PFC emulsion and possibly enhanced nitrogen washout through NO-increased blood flow rate and/or the removal of endothelial micro bubble nuclei precursors. Previous reports have shown that metabolic gases (i.e., oxygen in particular) and water vapor contribute to bubble growth and stabilization during altitude exposures. Accordingly, we hypothesize that the administration of PFC and NO donors upon hypobaric pressure exposures either (1) enhance the bubble disappearance rate through faster desaturation of nitrogen, or in contrast (2) promote bubble growth and stabilization through an increased oxygen supply.

Methods

In anesthetized rats, micro air bubbles (containing 79 % nitrogen) of 4–500 nl were injected into exposed abdominal adipose tissue. Rats were decompressed in 36 min to 25 kPa (~10,376 m above sea level) and bubbles studied for 210 min during continued oxygen breathing (F_IO₂ = 1). Rats were administered PFC, NO, or combined PFC and NO.

Results

In all groups, most bubbles grew transiently, followed by a stabilization phase. There were no differences in the overall bubble growth or decay between groups or when compared with previous data during oxygen breathing alone at 25 kPa.

Conclusion

During extreme altitude exposures, the contribution of metabolic gases to bubble growth compromises the therapeutic effects of PFC and NO, but PFC and NO do not induce additional bubble growth.     

Effect of isobaric breathing gas shifts from air to heliox mixtures on resolution of air bubbles in lipid and aqueous tissues of recompressed rats

Deep tissue isobaric counterdiffusion that may cause unwanted bubble formation or transient bubble growth has been referred to in theoretical models and demonstrated by intravascular gas formation in animals, when changing inert breathing gas from nitrogen to helium after hyperbaric air breathing. We visually followed the in vivo resolution of extravascular air bubbles injected at 101 kPa into nitrogen supersaturated rat tissues: adipose, spinal white matter, skeletal muscle or tail tendon. Bubbles were observed during isobaric breathing-gas shifts from air to normoxic (80:20) heliox mixture while at 285 kPa or following immediate recompression to either 285 or 405 kPa, breathing 80:20 and 50:50 heliox mixtures. During the isobaric shifts, some bubbles in adipose tissue grew marginally for 10–30 min, subsequently they shrank and disappeared at a rate similar to or faster than during air breathing. No such bubble growth was observed in spinal white matter, skeletal muscle or tendon. In spinal white matter, an immediate breathing gas shift after the hyperbaric air exposure from air to both (80:20) and (50:50) heliox, coincident with recompression to either 285 or 405 kPa, caused consistent shrinkage of all air bubbles, until they disappeared from view. Deep tissue isobaric counterdiffusion may cause some air bubbles to grow transiently in adipose tissue. The effect is marginal and of no clinical consequence. Bubble disappearance rate is faster with heliox breathing mixtures as compared to air. We see no reason for reservations in the use of heliox breathing during treatment of air-diving-induced decompression sickness.     

Effect of pre-breathing oxygen at different depth on oxidative status and calcium concentration in lymphocytes of scuba divers

Aim: In‐water pre‐breathing oxygen at various depths reduces decompression‐induced bubble formation and platelet activation, but it could induce side effects such as oxidative stress. The aim of this study was to investigate the effect of in‐water pre‐breathing oxygen, at different depths, on the oxidative status and intracellular calcium ([Ca²⁺]i) of peripheral blood lymphocytes isolated from six divers. They participated in a 4‐diving protocol. Two week recovery time was allowed between successive dives. Before diving, all divers, for 20 min, breathed normally at sea level (dive 1), 100% oxygen at sea level (dive 2), 100% oxygen at 6 msw (dive 3), 100% oxygen at 12 msw (dive 4). Then they dived to 30 msw for 20 min with air tank. Methods: Blood samples were collected before and after each dive. Hydrogen peroxide (H₂O₂) levels, catalase (CAT) activity, mRNA expression of CAT, glutathione peroxidase (GPx) and superoxide dismutase (SOD), and the [Ca²⁺]i in lymphocytes were measured. Results: The dives slightly decreased lymphocyte number and significantly reduced lymphocyte H₂O₂ levels. CAT activity was higher after scuba diving and, dive 3 enhanced mRNA gene expression of CAT, GPx and SOD. The [Ca²⁺]i was higher after dive 1 and 2 than pre‐diving, while was maintained at pre‐diving value after dive 3 and 4. Conclusion: Our results suggest that pre‐breathing oxygen, in particular at 12 msw, may enhance lymphocyte antioxidant activity and reduce reactive oxygen species levels. Pre‐breathing oxygen in water may also preserve calcium homeostasis, suggesting a protective role in the physiological lymphocyte cell functions.     

Diving decompression models and bubble metrics: Modern computer syntheses

A quantitative summary of computer models in diving applications is presented, underscoring dual phase dynamics and quantifying metrics in tissue and blood. Algorithms covered include the multitissue, diffusion, split phase gradient, linear-exponential, asymmetric tissue, thermodynamic, varying permeability, reduced gradient bubble, tissue bubble diffusion, and linear-exponential phase models. Defining relationships are listed, and diver staging regimens are underscored. Implementations, diving sectors, and correlations are indicated for models with a history of widespread acceptance, utilization, and safe application across recreational, scientific, military, research, and technical communities. Presently, all models are incomplete, but many (included above) are useful, having resulted in diving tables, underwater meters, and dive planning software. Those herein employ varying degrees of calibration and data tuning. We discuss bubble metrics in tissue and blood as a backdrop against computer models. The past 15 years, or so, have witnessed changes and additions to diving protocols and table procedures, such as shorter nonstop time limits, slower ascent rates, shallow safety stops, ascending repetitive profiles, deep decompression stops, helium based breathing mixtures, permissible reverse profiles, multilevel techniques, both faster and slower controlling repetitive tissue halftimes, smaller critical tensions, longer flying-after-diving surface intervals, and others. Stimulated by Doppler and imaging technology, table and decompression meter development, theory, statistics, chamber and animal testing, or safer diving consensus, these modifications affect a gamut of activity, spanning bounce to decompression, single to multiday, and air to mixed gas diving. As it turns out, there is growing support for many protocols on operational, experimental, and theoretical grounds, with bubble models addressing many concerns on plausible bases, but with further testing or profile data analyses requisite.     

Exercise-induced myofibrillar disruption with sarcolemmal integrity prior to simulated diving has no effect on vascular bubble formation in rats

Decompression sickness is initiated by gas bubbles formed during decompression, and it has been generally accepted that exercise before decompression causes increased bubble formation. There are indications that exercise-induced muscle injury seems to be involved. Trauma-induced skeletal muscle injury and vigorous exercise that could theoretically injure muscle tissues before decompression have each been shown to result in profuse bubble formation. Based on these findings, we hypothesized that exercise-induced skeletal muscle injury prior to decompression from diving would cause increase of vascular bubbles and lower survival rates after decompression. In this study, we examined muscle injury caused by eccentric exercise in rats prior to simulated diving and we observed the resulting bubble formation. Female Sprague–Dawley rats (n = 42) ran downhill (?16º) for 100 min on a treadmill followed by 90 min rest before a 50-min simulated saturation dive (709 kPa) in a pressure chamber. Muscle injury was evaluated by immunohistochemistry and qPCR, and vascular bubbles after diving were detected by ultrasonic imaging. The exercise protocol resulted in increased mRNA expression of markers of muscle injury; αB-crystallin, NF-κB, and TNF-α, and myofibrillar disruption with preserved sarcolemmal integrity. Despite evident myofibrillar disruption after eccentric exercise, no differences in bubble amounts or survival rates were observed in the exercised animals as compared to non-exercised animals after diving, a novel finding that may be applicable to humans.     

Statistical correlations and risk analyses techniques for a diving dual phase bubble model and data bank using massively parallel supercomputers

Linking model and data, we detail the LANL diving reduced gradient bubble model (RGBM), dynamical principles, and correlation with data in the LANL Data Bank. Table, profile, and meter risks are obtained from likelihood analysis and quoted for air, nitrox, helitrox no-decompression time limits, repetitive dive tables, and selected mixed gas and repetitive profiles. Application analyses include the EXPLORER decompression meter algorithm, NAUI tables, University of Wisconsin Seafood Diver tables, comparative NAUI, PADI, Oceanic NDLs and repetitive dives, comparative nitrogen and helium mixed gas risks, USS Perry deep rebreather (RB) exploration dive,world record open circuit (OC) dive, and Woodville Karst Plain Project (WKPP) extreme cave exploration profiles. The algorithm has seen extensive and utilitarian application in mixed gas diving, both in recreational and technical sectors, and forms the bases forreleased tables and decompression meters used by scientific, commercial, and research divers. The LANL Data Bank is described, and the methods used to deduce risk are detailed. Risk functions for dissolved gas and bubbles are summarized. Parameters that can be used to estimate profile risk are tallied. To fit data, a modified Levenberg-Marquardt routine is employed with L2 error norm. Appendices sketch the numerical methods, and list reports from field testing for (real) mixed gas diving. A Monte Carlo-like sampling scheme for fast numerical analysis of the data is also detailed, as a coupled variance reduction technique and additional check on the canonical approach to estimating diving risk. The method suggests alternatives to the canonical approach. This work represents a first time correlation effort linking a dynamical bubble model with deep stop data. Supercomputing resources are requisite to connect model and data in application.     

Exercise and nitric oxide prevent bubble formation: a novel approach to the prevention of decompression sickness?

Nitrogen dissolves in the blood during dives, but comes out of solution if divers return to normal pressure too rapidly. Nitrogen bubbles cause a range of effects from skin rashes to seizures, coma and death. It is believed that these bubbles form from bubble precursors (gas nuclei). Recently we have shown that a single bout of exercise 20 h, but not 48 h, before a simulated dive prevents bubble formation and protects rats from severe decompression sickness (DCS) and death. Furthermore, we demonstrated that administration of N ^ω-nitro- l -arginine methyl ester, a non-selective inhibitor of NO synthase (NOS), turns a dive from safe to unsafe in sedentary but not exercised rats. Therefore based upon previous data an attractive hypothesis is that it may be possible to use either exercise or NO-releasing agents before a dive to inhibit bubble formation and thus protect against DCS. Consequently, the aims of the present study were to determine whether protection against bubble formation in 'diving' rats was provided by (1) chronic and acute administration of a NO-releasing agent and (2) exercise less than 20 h prior to the dive. NO given for 5 days and then 20h prior to a dive to 700 kPa lasting 45 min breathing air significantly reduced bubble formation and prevented death. The same effect was seen if NO was given only 30 min before the dive. Exercise 20h before a dive surpressed bubble formation and prevented death, with no effect at any other time (48, 10, 5 and 0.5h prior to the dive). Pre-dive activities have not been considered to influence the growth of bubbles and thus the risk of serious DCS. The present novel findings of a protective effect against bubble formation and death by appropriately timed exercise and an NO-releasing agent may form the basis of a new approach to preventing serious decompression sickness.     

Differential effects on nitric oxide synthase, heat shock proteins and glutathione in human endothelial cells exposed to heat stress and simulated diving

Decompression sickness (DCS) may result from damage to the endothelium caused by the gas bubbles formed during decompression and may be related to nitric oxide (NO) production by nitric oxide synthase (NOS). Heat stress prior to diving has been shown to protect animals from DCS, and by simulating this treatment in human endothelial cells (HUVEC) we have shown that a simulated dive performed subsequent to a heat stress potentiated the heat-induced expression of HSP70 and increased the level of the antioxidant glutathione (GSH). Since operational saturation diving is performed at an increased oxygen level, HUVEC have been exposed to heat stress and simulated diving at 40 kPa O(2), comparing the response on HSP70, HSP90 and GSH level to the effects previously observed at 20 kPa O(2). In addition, we wanted to investigate the effect on both endothelial NOS (eNOS) protein and enzymatic activity. The present results showed that a heat stress (45°C, 1 h) decreased the NOS activity and the protein markedly. Hyperoxia (40 kPa) alone or a dive either at 20 or 40 kPa O(2),had no effects on NOS activity or protein. At 40 kPa O(2) a simulated dive after heat stress potentiated the HS-induced HSP70 response, whereas the heat-induced HSP90 response decreased. GSH levels were found to be inversely related to NOS activity and protein expression, and might be explained by a possible post-translational regulation by glutathionylation of eNOS protein. The results add to the limited knowledge of these critical factors in cellular defence mechanisms that can prevent injury during decompression.     

Hyperoxia but not ambient pressure decreases tetrahydrobiopterin level without affecting the enzymatic capability of nitric oxide synthase in human endothelial cells

Nitric oxide (NO) seems to be related to bubble formation and endothelial dysfunction resulting in decompression sickness. Bubble formation can be affected by aerobic exercise or manipulating NO. A prior heat stress (HS) has been shown to confer protection against decompression sickness in rats. An important question was if the oxidative environment experienced during diving limits the availability of the nitric oxide synthase (NOS) cofactor tetrahydrobiopterin (BH4). Human endothelial cells were used to investigate how HS and simulated diving affected NO synthesis and defense systems such as heat shock protein 70 (HSP70) and glutathione (GSH). BH4 was measured using a novel LC–MS/MS method and NOS by monitoring the conversion of radiolabeled l-arginine to l-citrulline. Increased pO₂ reduced BH4 levels in cells in a dose-dependent manner independently of high pressure. This effect may result in decreased generation of NO by NOS. The BH4 decrease seemed to be abolished when cells were exposed to HS prior to hyperoxia. NOS enzyme was unaffected by increased pO₂ but substantially reduced after HS. The BH4 level seemed to a minor extent to be dependent upon GSH and probably to a higher degree dependent on other antioxidants such as ascorbic acid. A simulated dive at 60 kPa O₂ had a potentiating effect on the heat-induced HSP70 expression, whereas GSH levels were unaffected by hyperoxic exposure. HS, hyperoxia, and dive affected several biochemical parameters that may play important roles in the mechanisms protecting against the adverse effects of saturation diving.     

Workplace substance abuse prevention and help seeking: comparing team-oriented and informational training

Employees fail to seek help for alcohol or drug (AOD) abuse because of unhealthy work climates, stigma, and distrust in Employee Assistance Programs (EAPs). To address such problems, the authors randomly assigned groups of municipal employees (N = 260) to 2 types of training: a 4-hr informational review of EAPs and policy and an 8-hr training that embedded messages about AOD reduction in the context of team building and stress management. Pre- and posttraining and 6-month follow-up surveys assessed change. Group privacy regulation, EAP trust, help seeking, and peer encouragement increased for team training. Stigma of substance users decreased for information training. EAP/policy knowledge increased for both groups. A control group showed little change. Help seeking and peer encouragement also predicted EAP utilization. Integrating both team and informational training may be the most effective for improving help seeking and EAP utilization.     

Exercise before and after SCUBA diving and the role of cellular microparticles in decompression stress

Risk in SCUBA diving is often associated with the presence of gas bubbles in the venous circulation formed during decompression. Although it has been demonstrated time-after-time that, while venous gas emboli (VGE) often accompany decompression sickness (DCS), they are also frequently observed in high quantities in asymptomatic divers following even mild recreational dive profiles. Despite this VGE are commonly utilized as a quantifiable marker of the potential for an individual to develop DCS. Certain interventions such as exercise, antioxidant supplements, vibration, and hydration appear to impact VGE production and the decompression process. However promising these procedures may seem, the data are not yet conclusive enough to warrant changes in decompression procedure, possibly suggesting a component of individual response. We hypothesize that the impact of exercise varies widely in individuals and once tested, recommendations can be made that will reduce individual decompression stress and possibly the incidence of DCS. The understanding of physiological adaptations to diving stress can be applied in different diseases that include endothelial dysfunction and microparticle (MP) production.Exercise before diving is viewed by some as a protective form of preconditioning because some studies have shown that it reduces VGE quantity. We propose that MP production and clearance might be a part of this mechanism. Exercise after diving appears to impact the risk of adverse events as well. Research suggests that the arterialization of VGE presents a greater risk for DCS than when emboli are eliminated by the pulmonary circuit before they have a chance to crossover. Laboratory studies have demonstrated that exercise increases the incidence of crossover likely through extra-cardiac mechanisms such as intrapulmonary arterial-venous anastomoses (IPAVAs). This effect of exercise has been repeated in the field with divers demonstrating a direct relationship between exercise and increased incidence of arterialization.     

No changes in lung function after a saturation dive to 2.5 MPa with intermittent reduction in P_{{{{\rm O}}_{{{\rm 2}}} }} during decompression

Decompression stress and exposure to hyperoxia may cause a reduction in transfer factor of the lung for carbon monoxide and in maximal aerobic capacity after deep saturation dives. In this study lung function and exercise capacity were assessed before and after a helium–oxygen saturation dive to a pressure of 2.5 MPa where the decompression rate was reduced compared with previous deep dives, and the hyperoxic exposure was reduced by administering oxygen intermittently at pressures of 50 and 30 kPa during decompression. Eight experienced divers of median age 41 years (range 29–48) participated in the dive. The incidence of venous gas microemboli was low compared with previous deep dives. Except for one subject having treatment for decompression sickness, no changes in lung function or angiotensin converting enzyme, a marker of pulmonary endothelial cell damage, were demonstrated. The modified diving procedures with respect to decompression rate and hyperoxic exposure may have contributed to the lack of changes in lung function in this dive compared with previous deep saturation dives.     

Assessment of spinal cord trauma using evoked potentials in a rat model of decompression sickness

A rapid quantitative technique for assessing spinal cord trauma in a rat model of decompression sickness is described. Evoked potentials are measured from the lower limbs of rats before and after dives with compressed air in a hyperbaric chamber. Under chloral hydrate anesthesia, the sciatic nerve is stimulated at the sciatic notch with needle electrodes and platinum/iridium electrodes are used to record the action potentials from the plantar muscles. Analysis showed that the sensory reflex response was markedly depressed in the rats soon after diving and did not recover for up to 5 days. The motor response was similarly affected although to a lesser degree. The latency of the reflex response also became prolonged after 3 days. The significant and complex pattern of neurological dysfunction shown by this electrophysiologic technique validates the use of the rat model for the study of spinal cord decompression sickness. This technique should aid studies aimed at testing new therapies for this disease.     

A role for oxygen-induced osmosis in hyperbaric oxygen therapy.

The principles of gas-induced osmosis, demonstrated in the 1970s, have been applied to the very large steady-state gradients of O2 arising between arterial blood and hypoxic tissue during hyperbaric oxygen (HBO) therapy to produce a fluid 'pump' in the desired direction for resolving accompanying oedema. Thus, in soft-tissue injuries, an oxygen-induced fluid pump would break the vicious cycle between ischaemia, hypoxia and oedema at the point of oedema rather than hypoxia, as hitherto assumed. This osmotic mechanism enables the successes of HBO therapy in hypoxic disorders to be reconciled with early failures in such areas as hyperbaric radiotherapy, where substitution of O2 for N2 in inspired air was clearly not reflected at the tissue level. This argument also applies to the success of HBO in treating air embolism and decompression sickness over simple compression. The oxygen pump would seem to offer a more plausible explanation for the success of HBO therapy than theories based upon O2 delivery by the circulation, especially when considering cardiovascular reflexes to elevated PaO2 and the marginal increase in blood O2 content upon switching to HBO from normobaric oxygen breathing.     

Effect of oxygen-breathing during a decompression-stop on bubble-induced platelet activation after an open-sea air dive

Purpose

We highlighted a relationship between decompression-induced bubble formation and platelet micro-particle (PMP) release after a scuba air-dive. It is known that decompression protocol using oxygen-stop accelerates the washout of nitrogen loaded in tissues. The aim was to study the effect of oxygen deco-stop on bubble formation and cell-derived MP release.

Methods

Healthy experienced divers performed two scuba-air dives to 30 msw for 30 min, one with an air deco-stop and a second with 100 % oxygen deco-stop at 3 msw for 9 min. Bubble grades were monitored with ultrasound and converted to the Kisman integrated severity score (KISS). Blood samples for cell-derived micro-particle analysis (AnnexinV for PMP and CD31 for endothelial MP) were taken 1 h before and after each dive.

Results

Mean KISS bubble score was significantly lower after the dive with oxygen-decompression stop, compared to the dive with air-decompression stop (4.3 ± 7.3 vs. 32.7 ± 19.9, p < 0.001). After the dive with an air-breathing decompression stop, we observed an increase of the post-dive mean values of PMP (753 ± 245 vs. 381 ± 191 ng/μl, p = 0.003) but no significant change in the oxygen-stop decompression dive (329 ± 215 vs. 381 +/191 ng/μl, p = 0.2). For the post-dive mean values of endothelial MP, there was no significant difference between both the dives.

Conclusions

The Oxygen breathing during decompression has a beneficial effect on bubble formation accelerating the washout of nitrogen loaded in tissues. Secondary oxygen-decompression stop could reduce bubble-induced platelet activation and the pro-coagulant activity of PMP release preventing the thrombotic event in the pathogenesis of decompression sickness.