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.

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.

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.

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.

Ascorbic acid supplementation diminishes microparticle elevations and neutrophil activation following SCUBA diving.

Predicated on evidence that diving-related microparticle generation is an oxidative stress response, this study investigated the role that oxygen plays in augmenting production of annexin V-positive microparticles associated with open-water SCUBA diving and whether elevations can be abrogated by ascorbic acid. Following a cross-over study design, 14 male subjects ingested placebo and 2-3 wk later ascorbic acid (2 g) daily for 6 days prior to performing either a 47-min dive to 18 m of sea water while breathing air (∼222 kPa N2/59 kPa O2) or breathing a mixture of 60% O2/balance N2 from a tight-fitting face mask at atmospheric pressure for 47 min (∼40 kPa N2/59 kPa O2). Within 30 min after the 18-m dive in the placebo group, neutrophil activation, and platelet-neutrophil interactions occurred, and the total number of microparticles, as well as subgroups bearing CD66b, CD41, CD31, CD142 proteins or nitrotyrosine, increased approximately twofold. No significant elevations occurred among divers after ingesting ascorbic acid, nor were elevations identified in either group after breathing 60% O2. Ascorbic acid had no significant effect on post-dive intravascular bubble production quantified by transthoracic echocardiography. We conclude that high-pressure nitrogen plays a key role in neutrophil and microparticle-associated changes with diving and that responses can be abrogated by dietary ascorbic acid supplementation.

Effect of in-water oxygen prebreathing at different depths on decompression-induced bubble formation and platelet activation.

Effect of in-water oxygen prebreathing at different depths on decompression-induced bubble formation and platelet activation in scuba divers was evaluated. Six volunteers participated in four diving protocols, with 2 wk of recovery between dives. On dive 1, before diving, all divers breathed normally for 20 min at the surface of the sea (Air). On dive 2, before diving, all divers breathed 100% oxygen for 20 min at the surface of the sea [normobaric oxygenation (NBO)]. On dive 3, before diving, all divers breathed 100% O2 for 20 min at 6 m of seawater [msw; hyperbaric oxygenation (HBO) 1.6 atmospheres absolute (ATA)]. On dive 4, before diving, all divers breathed 100% O2 for 20 min at 12 msw (HBO 2.2 ATA). Then they dove to 30 msw (4 ATA) for 20 min breathing air from scuba. After each dive, blood samples were collected as soon as the divers surfaced. Bubbles were measured at 20 and 50 min after decompression and converted to bubble count estimate (BCE) and numeric bubble grade (NBG). BCE and NBG were significantly lower in NBO than in Air [0.142+/-0.034 vs. 0.191+/-0.066 (P<0.05) and 1.61+/-0.25 vs. 1.89+/-0.31 (P<0.05), respectively] at 20 min, but not at 50 min. HBO at 1.6 ATA and 2.2 ATA has a similar significant effect of reducing BCE and NBG. BCE was 0.067+/-0.026 and 0.040+/-0.018 at 20 min and 0.030+/-0.022 and 0.020+/-0.020 at 50 min. NBG was 1.11+/-0.17 and 0.92+/-0.16 at 20 min and 0.83+/-0.18 and 0.75+/-0.16 at 50 min. Prebreathing NBO and HBO significantly alleviated decompression-induced platelet activation. Activation of CD62p was 3.0+/-0.4, 13.5+/-1.3, 10.7+/-0.9, 4.5+/-0.7, and 7.6+/-0.8% for baseline, Air, NBO, HBO at 1.6 ATA, and HBO at 2.2 ATA, respectively. The data show that prebreathing oxygen, more effective with HBO than NBO, decreases air bubbles and platelet activation and, therefore, may be beneficial in reducing the development of decompression sickness.

Decompression to altitude: assumptions, experimental evidence, and future directions.

Although differences exist, hypobaric and hyperbaric exposures share common physiological, biochemical, and clinical features, and their comparison may provide further insight into the mechanisms of decompression stress. Although altitude decompression illness (DCI) has been experienced by high-altitude Air Force pilots and is common in ground-based experiments simulating decompression profiles of extravehicular activities (EVAs) or astronauts' space walks, no case has been reported during actual EVAs in the non-weight-bearing microgravity environment of orbital space missions. We are uncertain whether gravity influences decompression outcomes via nitrogen tissue washout or via alterations related to skeletal muscle activity. However, robust experimental evidence demonstrated the role of skeletal muscle exercise, activities, and/or movement in bubble formation and DCI occurrence. Dualism of effects of exercise, positive or negative, on bubble formation and DCI is a striking feature in hypobaric exposure. Therefore, the discussion and the structure of this review are centered on those highlighted unresolved topics about the relationship between muscle activity, decompression, and microgravity. This article also provides, in the context of altitude decompression, an overview of the role of denitrogenation, metabolic gases, gas micronuclei, stabilization of bubbles, biochemical pathways activated by bubbles, nitric oxide, oxygen, anthropometric or physiological variables, Doppler-detectable bubbles, and potential arterialization of bubbles. These findings and uncertainties will produce further physiological challenges to solve in order to line up for the programmed human return to the Moon, the preparation for human exploration of Mars, and the EVAs implementation in a non-zero gravity environment.

Recompression during decompression and effects on bubble formation in the pig.

INTRODUCTION: There is a relationship between gas bubble formation in the vascular system and serious decompression sickness. Hence, control of the formation of vascular bubbles should allow safer decompression procedures. METHODS: There were 12 pigs that were randomly divided into an experimental group (EXP) and a control group (CTR) of 6 animals each. The pigs were compressed to 500 kPa (5 ATA) in a dry hyperbaric chamber and held for 90 min bottom time breathing air. CTR animals were decompressed according to a modified USN dive profile requiring four stops. EXP followed the same profile except that a 5-min recompression of 50 kPa (0.5 ATA) was added at the end of each of the last three decompression stops before ascending to the next stop depth. RESULTS: All CTR animals developed bubbles, compared with only one animal in EXP. The number of bubbles detected during and after the dive was 0.02 +/- 0.02 bubbles x cm(-2) in CTR, while the number of bubbles detected in EXP were 0.0009 +/- 0.005 bubbles x cm(-2); the difference was highly significant. CONCLUSION: By brief recompression during late decompression stops, the amount of bubbles was reduced. Our findings give further support for a gas phase model of decompression.

Decreased levels of PAI-1 and alpha 2-antiplasmin contribute to enhanced fibrinolytic activity in divers.

BACKGROUND: There are a number of reported cases of decompression sickness (DCS) with haemorrhages. These cases have not been sufficiently investigated and thus bleeding complications could not be directly correlated to the enhanced fibrinolysis. OBJECTIVES: The effect of hyperbaric exposition and decompression on the main components of fibrinolytic system has been measured. METHODS: Two groups of 25 male divers each were subjected to hyperbaric exposures to the pressure of either 400 kPa - group I - or 700 kPa - group II followed by a staged decompression. The divers were monitored for clinical symptoms of DCS and checked for Doppler-detected venous gas bubbles. Venous blood was drawn from divers before exposition and 15 min after decompression. The concentrations and activities of t-PA and PAI-1 as well as concentrations of PAP and alpha2-antiplasmin and activity of factor XIIa were measured. RESULTS: In all groups of divers no cases of DCS as well as detectable gas bubbles were noted. We observed elevated concentration of PAP, decreased concentration of alpha2-AP, decreased PAI-1 concentration and activity. There were no significant changes in factor XIIa activity as well as of t-PA concentration and activity. CONCLUSIONS: Hyperbaric exposition and decompression induce activation of fibrinolysis, even in the absence of detectable gas bubbles. Fibrinolytic activity increases mainly due to decrease of PAI-1 concentration and activity. Further clinical trials are necessary for the estimation of the importance of activation of fibrinolysis with decreased level of PAI-1 and alpha2-AP as a possible risk factor for bleeding in divers.

Cerebral artery blood velocity in normal subjects during acute decreases in barometric pressure.

To investigate the effect of acute changes in barometric pressure on regional cerebral perfusion we studied the middle cerebral artery (MCA) blood velocity in five healthy male volunteers by means of a low-pressure chamber. The MCA blood velocity, arterial blood and respiratory gases were measured at the barometric pressures of 1, 0.8, 0.65, and 0.5 atmospheres. The observed blood velocity (Vo) showed no systematic changes. Decreases in barometric pressure induced hypoxia and hypocapnia. When normalizing the MCA blood velocity (Vn) to a standard P(CO2) (5.3 kPa), thereby correcting for the hypoxic induced hypocapnia, we obtained an inverse relationship between cerebral artery blood velocity and arterial blood oxygen content (CaO2). The oxygen supply to the brain, estimated as the product of Vo and CaO2, decreased with lowering of the barometric pressure. However, the product of Vn and CaO2 remained constant. This suggests the existence of a regulatory mechanism attempting to maintain a constant oxygen supply to the brain during acute changes in CaO2, if the hyperventilation induced decrease in PCO2 can be omitted. In the artificial situation of a low pressure chamber, our findings are quite similar to those obtained at sea level. This indicates that the underlying mechanisms of control of cerebral blood flow do not change during acute exposure to altitude.

Cytokine response after acute hyperbaric exposure in the rat.

Intravascular gas has earlier been shown to activate leukocytes and platelets, enhance cell adhesion, and promote secretion of vasoactive substances from platelets. Since decompression is known to release gas bubbles in the bloodstream, the present study was undertaken to investigate the effect of a standardized decompression trauma on inflammatory mediators. Two series of experiments were performed in which male Wistar rats were subjected to a sublethal decompression trauma using a dry pressure chamber. Postdive measurements of cytokine levels were performed to look for signs of an inflammatory reaction. All animals subjected to a decompression trauma showed postdive signs of mild to severe decompression illness (DCI) and measurements of interleukin-6 (IL-6) indicated a postdive increase in the majority of these animals. Our finding of a postdive increase in IL-6 suggests that an inflammatory response, probably created by a blood-gas interface, may be a factor in the process leading to DCI.

Ruthenium red staining of blood-bubble interface in acute decompression sickness in rat.

The ultrastructure of the blood-bubble interface has been studied in rats decompressed experimentally. Subsequent to staining with ruthenium red there was detected by electron microscopy a continuous envelope like layer about 20 nm thick at the bubble-facing surface of the interface. The envelope like structure was visualized also by concanavalin A-ferritin, a glycosyl- and mannosyl residue-recognizing lectin coupled with an electron-dense probe, but the structure was not at all seen by the use of the conventional stains used in electron microscopy, uranyl acetate and lead citrate. No electron-dense layer was discernible on the application of only osmium tetroxide without further staining. The results indicate that material stainable by ruthenium red, and binding concanavalin A (probably a glycoprotein), is concentrated at the blood-bubble interface upon decompression. It is suggested that it plays a role in stabilization of the bubble and in the hematological alterations that are frequently observable in decompression sickness.

[Blood coagulation processes in decompression sickness and hyperbaric therapy]. / Processi emocoagulativi nella malattia da decompressione e nel trattamento iperbarico.

The hyperaggregability of platelets is remarkably important in the pathogenesis of decompression sickness. The basis of this phenomenon might consist of an excessive production of metabolites of arachidonic acid (C 20:4) whose action favours aggregation (prostaglandin endoperoxides PGG2 and PGH2 and Tromboxane A2) in respect of the synthesis of its derivatives exerting an antithrombotic action (prostacyclin I2). The antiaggregating therapy usually associated to the hyperbaric treatment involves administration of acetylsalicylic acid in low doses (3.5-5 mg/kg every three days), associated if necessary to dypyridamol. As a prophylaxis against thrombotic phenomena in "risky" subjects, a congruous dietetic assumption of polyunsaturated fatty acids is recommended, such as linoleic acid (C 18:2) and eicosapentaenoic acid (C 20:5) which are forerunners of anti-aggregating prostaglandin derivates. Hyperbaric oxygenation might finally lead to the production of lypid peroxides apt to inhibit the synthesis of PGI2. In such cases it is a rational procedure to administer vitamin E in high doses, as physiological antioxidant of lypids.