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PubMed2003

Hand discomfort following heliox chamber dives.

During a series of dry chamber dives using compressed heliox, five attendants and one wet diver experienced eight episodes of hand discomfort, the character of which was atypical of limb pain during decompression sickness. Although immersed for most of the dive, during the compression and decompression phases, the wet diver's hands were out of the water and hence exposed to the helium-containing chamber atmosphere. In all cases, symptoms resolved within a maximum of 48 h. There was no response to hyperbaric oxygen therapy in the three cases that presented before spontaneous resolution. While the attendants wore dry suits to minimize skin absorption of helium, their hands, were exposed to the heliox atmosphere. After the first six cases of hand symptoms, a dry glove assembly was added to prevent helium absorption through the exposed hand. Two cases of hand discomfort occurred following the addition of the dry glove assembly to the dry suit. In both cases, the symptoms were less severe and resolved over a significantly shorter time period. Adoption of the dry gloves resulted in the incidence of hand discomfort among attendants falling from 25% (5/20) to 2.4% (2/84) (p = 0.005). Possible mechanisms of causation of this hand discomfort, thought to be the result of local tissue absorption of helium, are discussed.

Administration, Cutaneous↗

PubMedDate not supplied

[Growth dynamics and the largest size of gas bubbles emerging in body tissues due to decompression].

Symptoms of decompression sickness (DCS) develop when the total volume of gas bubbles due to decompression reaches the magnitude critical for a body tissue. Number of the bubbles is a function of random nucleation intensity before, during or after decompression and tissue superaeration dynamics, whereas their size is unambiguously dependent on a tissue, decompression phase and bubbling time. A mathematical model of bubble tissue dynamics has been proposed for calculating the dynamics of mathematical expectation of the total gas in tissues and mounting a method for comparative analysis of the maximal DCS probability as a result of implementation of different decompression tables. Unequal intensity of nucleation during spaceflight EVA and its ground simulation w/o spacesuit is the course of inequality of decompression safety of these operations.

Decompression Sickness↗

PubMed1993

Breathing 100% oxygen compared with 50% oxygen: 50% nitrogen reduces altitude-induced venous gas emboli.

The risk of venous gas emboli (VGE) and decompression sickness (DCS) must be determined before selection of the lowest pressure for an extravehicular activity (EVA) pressure suit which eliminates the requirement for prebreathing. In earlier studies, use of a 50% oxygen:50% nitrogen breathing mixture (50:50 mix) during 139 zero-prebreathe decompressions of male subjects to 8.3-7.8 psia resulted in 51 instances of severe VGE and one case of DCS. Our current study investigated effects of 40 zero-prebreathe decompressions of male subjects to 8.3-6.8 psia for 6 h while breathing 100% oxygen and performing moderate exercise. No DCS symptoms were observed. Severe VGE were not detected at 8.3 psia, but were present during 10%, 20%, and 40% of the exposures at 7.8, 7.3, and 6.8 psia, respectively. Zero-prebreathe decompression while breathing 100% oxygen results in significantly lower VGE and DCS risk levels than while breathing a 50:50 mix. Our results show that 7.3 psia EVA pressure suits with 100% oxygen should be safer than 8.3 psia suits with a 50:50 mix.

Aerospace Medicine↗

PubMedDate not supplied

Evaluation of safety of hypobaric decompressions and EVA from positions of probabilistic theory.

Formation and subsequent evolution of gas bubbles in blood and tissues of subjects exposed to decompression are casual processes in their nature. Such character of bubbling processes in a body predetermines probabilistic character of decompression sickness (DCS) incidence in divers, aviators and astronauts. Our original probabilistic theory of decompression safety is based on stochastic models of these processes and on the concept of critical volume of a free gas phase in body tissues. From positions of this theory, the probability of DCS incidence during single-stage decompressions and during hypobaric decompressions under EVA in particular, is defined by the distribution of possible values of nucleation efficiency in "pain" tissues and by its critical significance depended on the parameters of a concrete decompression. In the present study the following is shown: 1) the dimensionless index of critical nucleation efficiency for "pain" body tissues is a more adequate index of decompression stress in comparison with Tissue Ratio, TR; 2) a priory the decompression under EVA performed according to the Russian protocol is more safe than decompression under EVA performed in accordance with the U.S. protocol; 3) the Russian space suit operated at a higher pressure and having a higher "rigidity" induces a stronger inhibition of mechanisms of cavitation and gas bubbles formation in tissues of a subject located in it, and by that provides a more considerable reduction of the DCS risk during real EVA performance.

Aerospace Medicine↗

PubMed2026

Adaptations to breath-hold diving: from traditional divers to elite athletes.

Breath-hold diving exposes humans to repeated episodes of profound hypoxia and hypercapnia, eliciting physiological adaptations that enable prolonged underwater performance. This article summarises current knowledge on chronic adaptations in elite breath-hold athletes and traditional diving populations, including the Bajau sea nomads of Southeast Asia and the Korean Haenyeo divers. Evidence indicates that repeated apnoea induces adaptations across multiple physiological systems. Haematological changes include increased spleen size and enhanced splenic contraction, augmenting circulating haemoglobin and oxygen stores during apnoea. In elite divers, structured training can increase resting spleen volume, whereas the Bajau exhibit genetically associated splenic enlargement linked to variants near the PDE10A gene. Cardiopulmonary adaptations include modified pulmonary vascular responses to hypoxia, improved oxygen conservation, and metabolic shifts favoring efficient mitochondrial energy production. Molecular adaptations involve enhanced antioxidant defenses and activation of hypoxia-responsive pathways that may mitigate oxidative stress associated with repeated hypoxia-reoxygenation cycles. Emerging evidence also suggests neural plasticity and possible structural brain adaptations, although the long-term neurological consequences of chronic intermittent hypoxia exposure remain uncertain. Studies of traditional diving populations indicate that both phenotypic plasticity and genetic selection contribute to diving capacity, highlighting interactions between training and evolution. Despite these benefits, breath-hold diving also carries risks, including hypoxic blackout, decompression sickness, and potential neurological injury. Understanding the mechanisms underlying human tolerance to extreme hypoxia may have implications beyond diving physiology, including applications in cardiovascular medicine, hypoxic diseases, and rehabilitation. Further longitudinal, genomic, and mechanistic studies are needed to clarify the limits, benefits, and clinical relevance of these adaptations.

Humans↗

PubMed1975

Evaluation of ultrasonic bubble detectors in vitro using calibrated microbubbles at selected velocities.

Two standard Doppler ultrasonic devices, currently used for detecting bubbles in vivo, have been evaluated and compared in vitro using carefully calibrated uniform micro-bubbles rising at terminal velocity through a static aqueous medium. Two unexpected findings were observed: (a) the focal length of the transducer apparently decreases for smaller bubble sizes, and (b) a significant horizontal convection current was produced by one of the instruments. When the medium was in motion, it was found that the sensitivity varied markedly with bubble velocity, varying from a minimum detectable diameter of 40 mum at 55 cm/sec to 170 mum at 20 cm/sec. These findings are discussed with regard to the limitations of the Doppler technique for monitoring gas emboli in vivo and as an early warning for decompression sickness in divers.

Decompression Sickness↗

PubMed1987

Increase in blood-brain barrier permeability by altitude decompression.

Previous studies indicated that exposure to compression-decompression increases blood-brain barrier (BBB) permeability to vital dyes and antibiotics. This report concerns functional and ultrastructural BBB changes induced by altitude decompression. A 2% trypan blue solution was intravenously injected (4 ml.kg-1) into 29 experimental and 19 control rabbits. Some animals also received horseradish peroxidase. The experimental animals were subjected to 30,000 ft (4.3 psi) for 45 min. Controls were kept at ground level. The animals were sacrificed 90 min postinjection. Gross and microscopic examination and spectrophotometric dye determination revealed significantly greater tracer penetration in experimental brains (mean dye concentration 27.06 +/- 4.42 micrograms.g-1) than in controls (4.52 +/- 1.52 micrograms.g-1). No sex differences were noted. Electron microscopy suggested that the increased BBB permeability was due to transendothelial vesicular transport and, occasionally, to penetration through interendothelial junctions. These observations may have relevance to pharmacotherapy in space and at high altitudes and to the pathogenesis of altitude decompression sickness.

Altitude Sickness↗

PubMed2004

[Treatment of acute cochleovestibular damage after diving].

BACKGROUND: There has been a steady in-crease of recreational scuba divers in the last years. The majority of diving associated diseases involve otorhinolaryngology, the most important of which are cochleovestibular dysfunctions as these can lead to permanent inner ear failure. MATERIAL AND METHODS: We discuss the origin and clinical symptoms, as well as the therapy, of both inner ear barotrauma and inner ear decompression illness. Our own experiences are considered together with a review of the literature from the last decade. RESULTS: Inner ear decompression illness seems to be a relatively common diving associated incident and is not as rare as previously thought. DISCUSSION: Hyperbaric oxygen therapy is the treatment of choice for patients with inner ear decompression sickness, but is contraindicated in patients with inner ear barotrauma. As long as an inner ear decompression illness can not be ruled out, we suggest that every patient should be treated using hyperbaric oxygen therapy but only after bilateral paracentesis.

Barotrauma↗

PubMed1976

Gas phase separation during decompression in man: ultrasound monitoring.

During two dive series, one to 132 fsw and one to 210 fsw, Doppler ultrasonic bubble detectors were used to monitor venous gas bubbles in divers during decompression and for 30 min thereafter. Various decompression schedules were used. Bubble scores were evaluated by independent listerners to tape recordings in a blind manner. A significant increase in bubble scores throughout the stages of decompression and postdecompression was demonstrated as well as a statistically significant relationship between bubble score and decompression sickness. A reduction in mean bubble score was found in divers who made an additional deep decompression stop that was unrelated to the extension of the decompression time. The implications of these findings are discussed.

Adult↗

PubMed1997

Reversibility in blood-brain barrier, microcirculation, and histology in rat brain after decompression.

To examine the changes in blood-brain barrier (BBB), cerebral microcirculation, and histology from 15 min to 72 h after decompression, 90 rats were exposed to experimental compression to 6 atm abs air for 90 min and subsequent rapid decompression. The disruption of BBB was examined by Evans blue extravasation. The cerebral microcirculation was demonstrated by perfusion with India ink. The area stained with Evans blue and the regions of defective filling with India ink, observed immediately after decompression decreased in size with time and were undetectable 3-24 h after decompression. The edematous brain tissue with enlarged perivascular space and darkly stained nerve cells also decreased to the uncompressed control level 1-24 h after decompression. These reversible dysbaric changes, however, reappeared 48-72 h after decompression. The different mechanisms, the physicochemical effects of microbubbles, and the maturation phenomenon after temporary brain ischemia induced by dysbaric microbubbles may be involved in the brain damage after decompression sickness.

Animals↗

PubMed1995

[A mathematical model of permissible integral supercritical supersaturation of tissues by gases under decompression].

A criterion of permissible integral supercritical gas oversaturation of the body tissues was established using mathematical modelling. The heart of this criterion is that if integral supercritical oversaturation of tissues by gases does not go beyond a permissible level, gas bubbles do not reach critical volumes and give rise to decompression sickness symptoms. An equation was also built to calculate integral supercritical oversaturation of tissues during and after decompression. Permissible integral supercritical saturation values were determined for animals from mice to dogs and humans basing on literary threshold pressures with saturation and follow-on one-step decompression.

Animals↗

PubMed1996

Hydrogenase encapsulation into red blood cells and regeneration of electron acceptor.

Biochemical decompression has been proposed as a method for reducing the amount of time required for deep-sea divers to return to the surface. Divers breathing H2/O2 mixtures would be presented with hydrogenase enzyme, and decompression would be accelerated by means of the enzymic removal of excess H2 from the tissues. We have studied FAD as a hydrogenase electron acceptor that is capable of transferring electrons derived from H2 oxidation directly to O2. Kinetic activity constants for the soluble hydrogenase from the bacterium Alcaligenes eutrophus H16 were determined with FAD, FMN and riboflavin as electron acceptors, and these values were compared with those obtained with the physiological electron acceptor NAD+. The Michaelis constants (K(m)) were similar for FAD, FMN and NAD. However, the maximal catalytic-centre activity (Kcat) was much lower for the flavins, and the catalytic efficiency (Kcat/K(m)) with FAD was 1/20th the value for NAD+. After enzyme-catalysed FAD reduction to FADH2, the FAD could be regenerated by addition of O2 and reduced again by the enzyme in the presence of H2. Thus FAD served as a regenerable electron shuttle between H2 and O2. H2O2, a by-product of FADH2 oxidation by O2, inhibited the enzyme. Much greater inhibition was observed with the reduced form of the enzyme. Active hydrogenase was efficiently encapsulated into human and pig red blood cells. Hydrogen consumption was seen with lysed carrier cells, but was demonstrated with unlysed carrier cells only when FAD was co-encapsulated along with enzyme. These results demonstrate that red blood cells encapsulating hydrogenase and FAD act as a system for continuous H2 consumption in a mammalian tissue without addition of exogenous factors, and such cells may provide a biotherapeutic method for reducing the risk and treatment of decompression sickness.

Animals↗

PubMed1984

A theoretical method for selecting space craft and space suit atmospheres.

A theoretical method for selecting space craft and space suit atmospheres assumes that gas bubbles cause decompression sickness and that the risk increases when a critical bubble volume is exceeded. The method is consistent with empirical decompression exposures for humans under conditions of nitrogen equilibrium between the lungs and tissues. Space station atmospheres are selected so that flight crews may decompress immediately from sea level to station pressure without preoxygenation. Bubbles form as a result of this decompression but are less than the critical volume. The bubbles are absorbed during an equilibration period after which immediate transition to suit pressure is possible. Exercise after decompression and incomplete nitrogen equilibrium are shown to increase bubble size, and limit the usefulness of one previously tested stage decompression procedure for the Shuttle. The method might be helpful for evaluating decompression procedures before testing.

Decompression Sickness↗

PubMed1996

Complement system response to decompression.

A role for the activated complement system in the pathogenesis of decompression sickness has recently been suggested. In this study we aimed at evaluating the response of the complement system to decompression in 24 human volunteers. A significant reduction was observed in the levels of iC3, which is a conformationally changed form of the third complement component (C3), and C3A after decompression (P < 0.001). The levels of total C3 did not change during the experiment. A relatively mild decompression has thus led to a distinct change in the complement activation profile in human volunteers.

Adult↗

PubMed1982

The sport diving employee.

As scuba diving becomes an increasingly popular recreational activity, the probability of the occupational health physician seeing diving-related disorders increases. Recognition of many of these disorders is unlikely if not specifically looked for and if any account of diving activities is not forth-coming. Diagnosis and management of diving diseases range from simple ear squeeze to decompression sickness. There are relative and absolute contradictions to sport diving.

Decompression Sickness↗

PubMed1986

Respiratory mechanics in men following a deep air dive.

The mechanical properties of the lungs were measured in 10 men before and after a simulated air dive to 285 ft of seawater (87 m). The objective was to determine whether a dive likely to produce pulmonary bubble emboli would alter lung mechanics. Lung function was measured predive and at 1, 2, 3, 6, 7, and 23 h postdive. Measurements of lung function were also made at identical times on a control day when no dive was made. Each set of measurements included precordial Doppler signals, pulmonary resistance, quasistatic lung compliance, forced vital capacity (FVC), forced expired volume after 1.0 s (FEV 1.0), the ratio of FEV 1.0 to FVC (FEV 1.0/FVC%), and maximal airflow after 50 and 75% of the vital capacity had been expired (Vmax50 and Vmax75, respectively). Base-line measurements of pulmonary resistance and quasistatic compliance were normal in all subjects. FVC and FEV 1.0 were greater than predicted for most subjects and were increased proportionately so that the FEV 1.0/FVC% was normal. Following the dive, bubble signals were heard in four subjects, and two subjects had mild symptoms of decompression sickness. No subject demonstrated any alteration in lung function that could be attributed to the dive. We concluded that stressful decompressions capable of producing "silent" pulmonary bubble emboli do not alter lung mechanics.

Adult↗

PubMed1992

Retinal artery occlusion in a diver.

The clinical manifestation of decompression disorders is highly variable, ranging from mild rashes or joint pains to central nervous system symptoms like scotomata, paralysis and death. The diagnosis is easily overlooked, especially if an occupational history is not obtained. Recompression treatment with hyperbaric oxygen is the specific treatment for decompression sickness and air embolism. Prompt recognition and treatment are vital to recovery. However, there is a place for treatment of decompression disorders and embolism even when significant delay of up to 14 days has occurred. This case report discusses decompression disorders in relation to an unskilled fisherman diver who present with retinal artery occlusion. Decompression disorder leading to retinal artery occlusion is a very rare presentation. The difficulty of diagnosis is discussed as well as the result of delayed hyperbaric treatment.

Adult↗

PubMed2003

Diving up to 60 m depth followed by decompression has no effect on pro-enzyme and total thrombin activatable fibrinolysis inhibitor antigen concentration.

The aim of our study was to investigate the effect of two different hyperbaric exposures followed by decompression on thrombin activatable fibrinolysis inhibitor (TAFI) concentration and activity. The hyperbaric conditions correspond to diving to 30 and 60 m water depth. Thirty-four male divers were tested in decompression habitat LSH-200, with air as a breathing medium. The pro-enzyme and total TAFI antigen concentration were measured. We did not observed significant changes of either pro-enzyme or total TAFI antigen concentration after both series of exposures followed by decompression. The results may suggest that TAFI plays only a marginal role, if any, in the regulation of induced fibrinolysis in divers, which may contribute to bleeding episodes in a course of decompression sickness.

Adult↗