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At least 145 records · Page 8Linked to original sources
PubMed1995

Application of the mechanical oscillator technique to the investigation of EVA decompression.

The ultrasonic bubble detection technique has been used as a versatile tool in the investigation of hypobaric decompression procedures for the last two decades. However, this method can only detect relatively large bubbles > 30-50 micrometers (usually in venous blood) and not the very first stages of bubble formation. Recently, the mechanical oscillator technique has been applied in air diving trials in order to detect small blood density changes due to hypothetical fluid shifts. However, sharp density drops were found in the decompression process, and these have been attributed to gas bubble formation. In this study, this method was applied together with Doppler controls to a series of altitude decompressions to 300 and 500 hPa, which represents the range of EVA operational pressures currently used or planned. Six subjects participated in both series; the oscillator sample tube could be pressurized. By the application of pressure on a blood sample containing questionable gas bubbles, these are reduced in volume, like in recompression therapy, and thus the density of the sample is increased. This effect has been shown in all 6 subjects undergoing decompression to 300 hPa, whereas in the 500 hPa series only 3 out of 6 subjects corresponded with gas phase formation immediately after decompression. Typically, Doppler bubbles appeared only after some latency time between 20 and 60 min; after this time, the density effect had nearly vanished. It is concluded that the mechanical oscillator technique represents a complementary research instrument to the Doppler method, because it is able to deliver a quantitative resolution of the early stage of gas phase formation.

Aerospace Medicine↗
PubMed1976

Enhancement of base pair substitution induced by alkylating mutagens in simulated hyperbaric diving environments.

The effect of simulated saturated diving environments on mutagenicity was investigated using two histidine auxotrophs (hisG46 and hisTA1950 derived by Ames from Salmonella typhimurium LT2) exposed to several chemical mutagens. In agar diffusion tests with impregnated paper discs, 68 atm of normoxic supporting gases (containing 0.2 atm O2) reduced the number of histidine revertants of auxotrophs exposed to N-methyl-N'-nitro-N-nitrosoguanidine (NTG) and two other alkylating agents. The effect was induced in increasing order by helium, a mixture of neon and helium, nitrogen and argon. The effect of the gases on the growth of the two strains was small and did not explain the reduction of revertant recovery. On the other hand, it was shown that NTG in concentrations of 0.6 to 250 mug/ml was significantly more lethal for the hisG46 strain under 68 and 136 atm than at 1 atm. Revertant recovery was similarly related in both conditions. The maximal number of revertants, approx. 2.6 X 10(4), was obtained at 136 atm when the concentration of NTG was 0.6--1.25 mug/ml and at 1 atm when the concentration of NTG was 5--10 mug/ml. A comparable hydrostatic environment did not affect revertant recovery. The most plausible interpretation of these results is that hyperbaric environments accelerate the rate of intracellular accumulation of NTG, which is manifest in greater mutagenicity at the lower concentrations and greater lethality at all concentrations.

2-Aminopurine↗
PubMed2005

Validation of a gas chromatography/mass spectrometry method for the quantification of aerosolized Jet Propellant 8.

Jet Propellant 8 (JP-8) jet fuel is a kerosene-based fuel containing hundreds of hydrocarbons used by the military in NATO countries. Previous rodent inhalation studies carried out with aerosolized JP-8 never evaluated the exposure chamber atmosphere. For this reason, our laboratory developed an analytical method, with an accuracy of better than 80% and precision of better than 20%, for JP-8 aerosol and vapor samples using gas chromatography/mass spectrometry (GC/MS). A method was developed for quantification of selected individual components of JP-8 and for the total amount of JP-8 in aerosolized fuel. A 34 component surrogate hydrocarbon mixture (SHM) was developed and used for simultaneous analysis of the individual components. Three separate runs containing a standard curve and five replicates each at the selected concentrations were analyzed for both the SHM and neat JP-8. The resulting interday accuracy (100-percent relative error) and precision (relative standard deviation) values for the SHM were 86.5% or better and 8.0% or better, respectively. The intraday accuracy and precision values ranged from 99.29% to 84.50% and 0.97% to 12.4%, respectively. For the total amount of JP-8 in aerosol and vapor, the interday accuracy was 83.7% or better and interday precision was 7.0% or better. The intraday accuracy and precision values ranged from 94.8% to 80.4% and 2.4% to 10.5%, respectively. We then used this method to analyze samples collected from an inhalation chamber. From the data obtained, we are able to account for approximately 40-44% of the mass of the aerosol portion and 68-70% of the mass of the vapor portion. The aerosol represented 6-10% of the total mass of the aerosolized JP-8 fuel with the remaining portion being the vapor. From these experiments individual components were identified for further in vivo and in vitro toxicological testing.

Aerosols↗
PubMed2004

Transient exposure of rat pups to hyperoxia at normobaric and hyperbaric pressures does not cause retinopathy of prematurity.

We have shown that hyperoxia reduces brain damage in a rat model of hypoxia-ischemia. The purpose of this study was to examine the possibility of hyperoxia in inducing vision-threatening retinopathy. Two different experiments were conducted in this study. PART 1: seven-day-old rat pups were subjected to unilateral carotid artery ligation followed by 2 h of hypoxia (8% O2 at 37 degrees C). Pups were treated with 100% oxygen at 1 ATA, 1.5 ATA, and 3.0 ATA for a duration of 1 h. PART 2: Newborn rat pups were exposed to 100% oxygen at 1, 1.5, or 3.0 ATA for 1 h, the same treatment protocol used for brain protection after hypoxia-ischemia. Retinopathy was evaluated by the degree of neovascularization (measuring retinal vascular density), by the structural abnormalities (histology) in the retina, and by the expression of hypoxia-hyperoxia sensitive proteins including hypoxia-inducible factor-1alpha (HIF-1alpha) and vascular endothelial growth factor (VEGF) at 24 h, 1, 2, and 10 weeks after hyperoxia exposure. Hyperoxic treatment at all pressures administered significantly reduced the hypoxia-ischemic-induced reduction in brain weight. Retinal vascular density measurements revealed no signs of neovascularization after hyperoxia exposure. There were also no abnormalities in the structure of the retina and no changes in the protein expression of HIF-1alpha and VEGF following hyperoxia exposure. Exposure to hyperoxia for 1 h at normobaric or hyperbaric pressures did not result in the structural changes or abnormal vascularization that is associated with retinopathy of prematurity, suggesting that hyperoxia is a safe treatment for hypoxic newborn infants.

Analysis of Variance↗
PubMed2005

Evidence of a decrease in nitric oxide-storage molecules following acute hypoxia and/or hypobaria, by means of chemiluminescence analysis.

Nitrate, nitrite, and other nitroso compounds (NOxs) had been proposed as possible nitric oxide (NO) storage molecules. The present work examines, by means of chemiluminescence analysis, changes in NOx serum levels in rats 1 h before and 24, 48, and 72 h after exposure to acute hypobaric hypoxia (HH; barometric pressure [P(B)] 225 mmHg, oxygen partial pressure [PO2] 48 mmHg), normobaric hypoxia (NH; P(B) 716 mmHg [Jaén city], PO2 48 mmHg), hypobaric normoxia (HN; P(B) 225 mmHg, PO2 150 mmHg), and normobaric normoxia (NN; P(B) 716 mmHg, PO2 150 mmHg) the latter as a control group. Results show a decrease in NOx levels, which reached significance 24 h after exposure in HH animals, 4 h after exposure in the HN and NH groups, and persisted after 48 h of exposure in the HN group. NOx determinations were also performed in brain (cerebral cortex, hippocampus, decorticated brain [basal ganglia-brainstem] and cerebellum), liver, kidney, lung, and heart homogenates, 72 h after the experiment, to detect persistent effects when serum NOx levels had returned to basal values. Only in cerebellum (HN group) and hippocampus (HN and NH groups) were NOx levels significantly lower than in controls. We conclude that not only acute hypobaric hypoxia but also either hypobaria or hypoxia alone induce changes in NOx serum levels. Moreover, all three episodes involve a decrease in NOxs, greater and longer-lasting in hypoxia alone than in hypobaria and hypoxia together. The exhaustion of these NO-storage molecules could be critical when, as during a hypoxic episode, the L-arginine/NOS pathway is impaired.

Adaptation, Physiological↗
PubMed1998

Effect of hypobaria on ventilatory and CO2 responses to short-term hypoxic exposure in cats.

The effect of hypobaria on the ventilatory response to short-term hypoxia was studied by comparing the respiratory mechanical and inspired CO2 ventilatory responses to hypobaric hypoxia (438 mmHg) with normobaric hypoxia (11.8% FIO2). Fifteen spontaneously breathing, anesthetized cats were divided into three groups of five: time control, normobaric hypoxia and hypobaric hypoxia. Measurements of ventilation, gas exchange, and responses to intermittent CO2 rebreathing were collected over a 4 h period. PaO2 fell to 44.5 +/- 2.7 mmHg, PaCO2 fell to 24.8 +/- 0.9, and pH rose to 7.49 +/- 0.01 in both hypoxic groups. Tidal volume did not change with respect to time or condition, but frequency and ventilation were significantly increased in the hypobaric hypoxic group. The slope of the CO2 response was unchanged over time or by condition. These results suggest that hypobaric hypoxia may alter the pattern of breathing responses to hypoxia but not the CO2-response. If metabolic rate remained constant, these results could be explained by a difference in dead space between hypoxic conditions.

Animals↗
PubMed2001

Postural instability and acute mountain sickness during exposure to 24 hours of simulated altitude (4300 m).

Short exposures to severe or moderate hypoxia can have detrimental effects on postural stability. We hypothesized that continuous 24-h exposure to simulated 4300-m altitude (446 mmHg) would adversely affect postural stability and that this change in postural stability would be related to the severity of acute mountain sickness (AMS). On two different studies with similar experimental designs, postural instability was measured after approximately 3 and approximately 24 h of exposure using a computer-controlled unstable platform system in a total of 19 volunteers on three consecutive, 30-sec tests: eyes open (EO), eyes closed (EC), and a dynamic test involving tracking a circular moving object. Compared to baseline sea-level results, increases in postural instability were obtained with the EO test after 2 to 3 h (30%, p = 0.002) and 23 to 24 h (21%, p = 0.036) of altitude exposure. Similar increases were obtained on the EC test: 2 to 3 h (25%, p < 0.001) and 23 to 24 h (31%, p < 0.001). Although absolute instability values were higher on the EC test, the ratio EC/EO and the relative temporal changes with altitude exposure were similar. There were no significant altitude-stability effects on the target-tracking task. Sixty-three percent of the subjects (12 of 19) exhibited significant AMS (> 0.7 ESQ-C score) at some point during the 24-h exposure. No statistically significant correlations were obtained between the ESQ-C and any of the postural instability tests. These results indicate that postural stability is adversely affected during a 24-h exposure to 4300 m; however, there does not appear to be a correlation with the incidence or severity of AMS.

Adolescent↗
PubMed2000

Noninvasive assessment of cerebral oxygenation during acclimation to hypobaric hypoxia.

Factors regulating cerebral tissue PO2 (PtO2) are complex. With the increased use of clinical PtO2 monitors, it has become important to elucidate these mechanisms. The authors are investigating a new methodology (electron paramagnetic resonance oximetry) for use in monitoring cerebral PtO2 in awake animals over time courses of weeks. The authors used this to study cerebral PtO2 in rats during chronic acclimation to hypoxia predicting that such acclimation would cause an increase in PtO2 because of increases that occur in capillary density and oxygen carrying capacity. The average PtO2 between 7 and 21 days was increased by 228% over controls.

Acclimatization↗
PubMed1984

Norwegian deep diving trials.

In 1983 NUTEC, together with two diving companies, completed two dives with 12 divers (6 in each dive) to pressures equivalent to 350 m s.w., one dive lasted for 17 d, and the other, 24 d. The purpose of the dives was to demonstrate that the diving companies were prepared for diving to 300 m depth in the North Sea. No major medical or physiological problems arose during the dives, although all divers had minor symptoms of high pressure nervous syndrome during compressions. During decompression three decompression sickness incidents occurred, which involved pain only, and all were successfully treated. All divers went through comprehensive medical physiological examinations before and after the dives. No significant changes from values measured before diving have been found in the six divers who have so far been examined after diving, except that five of them were considerably more sensitive to CO2 after the dive than before. Several problems arose in connection with the divers' breathing equipment, thermal protection and communication, which need to be improved.

Atmosphere Exposure Chambers↗
PubMed2003

Hypobaric biology: Arabidopsis gene expression at low atmospheric pressure.

As a step in developing an understanding of plant adaptation to low atmospheric pressures, we have identified genes central to the initial response of Arabidopsis to hypobaria. Exposure of plants to an atmosphere of 10 kPa compared with the sea-level pressure of 101 kPa resulted in the significant differential expression of more than 200 genes between the two treatments. Less than one-half of the genes induced by hypobaria are similarly affected by hypoxia, suggesting that response to hypobaria is unique and is more complex than an adaptation to the reduced partial pressure of oxygen inherent to hypobaric environments. In addition, the suites of genes induced by hypobaria confirm that water movement is a paramount issue at low atmospheric pressures, because many of gene products intersect abscisic acid-related, drought-induced pathways. A motivational constituent of these experiments is the need to address the National Aeronautics and Space Administration's plans to include plants as integral components of advanced life support systems. The design of bioregenerative life support systems seeks to maximize productivity within structures engineered to minimize mass and resource consumption. Currently, there are severe limitations to producing Earth-orbital, lunar, or Martian plant growth facilities that contain Earth-normal atmospheric pressures within light, transparent structures. However, some engineering limitations can be offset by growing plants in reduced atmospheric pressures. Characterization of the hypobaric response can therefore provide data to guide systems engineering development for bioregenerative life support, as well as lead to fundamental insights into aspects of desiccation metabolism and the means by which plants monitor water relations.

Adaptation, Physiological↗
PubMed1982

Function of the Oxford Ventilator at high pressure.

The Penlon Oxford Ventilator functioned well to 6 atmospheres absolute in an air environment and to 31 atmospheres absolute in an oxyhelium environment, as assessed remotely utilising a lung ventilator performance analyser. It features easily comprehensible controls and functions, and its use in prolonged ventilatory support could be taught to non-anaesthetists with relative ease. In addition to its relative simplicity, it is reliable, readily available, and requires only fitting with a male Schrader valve for use at high pressures. The ventilator is recommended for ventilatory support under extreme hyperbaric conditions.

Air↗