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PubMed1992

Cochlear degeneration in guinea pigs after repeated hyperbaric exposures.

The effects of repeated hyperbaric exposures on inner ear function and morphology in guinea pigs were investigated with auditory electrophysiological testing, histopathological and electron microscopic techniques associated with enzyme histochemical method. The results showed that repeated hyperbaric exposures, though considered "safe," did cause damage to the cochlear system. Possible causes of the pathology include direct effects of repeated compression and decompression on the ear, and the possibility of inner ear decompression sickness and barotrauma cannot be excluded.

Animals↗
PubMed1998

Ocular bubble formation as a method of assessing decompression stress.

Tear film bubble formation and ultrasound reflectivity of the lens-vitreous humor compartments were monitored following simulated dives in a hyperbaric chamber. the sensitivity of these methods in determining decompression stress was compared with the results of precordial Doppler ultrasound. In addition, the utility of these diagnostic techniques in testing decompression dive profiles was evaluated. Eleven divers completed two series of chamber dives according to the decompression schedule of the Professional Association of Diving Instructors. The first dive series comprised dives to 70 feet of seawater (fsw) for 15, 29, and 40 min. The second series comprised maximum duration no-stop decompression dives to 40 fsw for 140 min, 70 fsw for 40 min, 90 fsw for 25 min, and 120 fsw for 13 min. Before and immediately after each dive, the following measurements were obtained from each subject: eye surface tear film bubble counts with a slit-lamp microscope, lens and vitreous humor reflectivity using A- and B-mode ophthalmic ultrasonic scan, and precordial Doppler ultrasonic detection of venous gas bubbles. Tear film bubble assessment and ocular scanning ultrasound were observed to be more sensitive in detecting decompression stress than the conventional Doppler ultrasonic surveillance of the precordial region. In contrast to precordial Doppler ultrasonic surveillance, which failed to detect any significant changes in circulating bubbles, tear film bubble formation displayed a dose-response relationship with increasing duration of the 70-fsw dives. Reflectivity changes of the lens-vitreous humor interface were not significant until the no-stop decompression limit was reached. In addition, for each of the no-stop decompression limit dives, increases in the average tear film bubble formation and lens-vitreous humor interface reflectivity were similar. Ocular bubble observations may provide a practical and objective ocular bubble index for analyzing existing decompression schedules and predicting individual susceptibility to decompression sickness.

Adolescent↗
PubMed2000

[Changes of glucocorticoid receptor in cerebral and hepatic cytosol during decompression stress injury in rats].

Objective. To observe the changes of glucocorticoid receptor (GR) in cerebral and hepatic cytosol during decompression stress injury in rats. Method. 30 rats were divided into 5 group. They were placed into the compression chamber for compression and decompression. The binding capacity of GR of cerebral and hepatic cytosol were measured by the exchange assay, using 3H dexamethasone as the ligand. Meanwhile, decompression bubbles on pericardial area were measured using Doppler ultrasonic method. Result. The binding capacity of GR of cerebral and hepatic cytosol reduced after decompression stress injury in the animals, especially cerebral cytosol (P<0.01, P<0.05). The result also showed that the binding capacity of cerebral and hepatic GR should have further decreased, if the therapeutic measure had not been used in animals suffered from decompression sickness (DCS). Conclusion. The changes of the binding capacity of GR of cerebral and hepatic cytosol were proved to be related to decompression stress injury, which might be taken as one of the indices for evaluating injury degree of DCS.

Animals↗
PubMed1997

Dibutyryl cAMP effects on thromboxane and leukotriene production in decompression-induced lung injury.

Decompression-induced venous bubble formation has been linked to increased neutrophil counts, endothelial cell injury, release of vasoactive eicosanoids, and increased vascular membrane permeability. These actions may account for inflammatory responses and edema formation. Increasing the intracellular cAMP has been shown to decrease eicosanoid production and edema formation in various models of lung injury. Reduction of decompression-induced inflammatory responses was evaluated in decompressed rats pretreated with saline (controls) or dibutyryl cAMP (DBcAMP, an analog of cAMP). After pretreatment, rats were exposed to either 616 kPa for 120 min or 683 kPa for 60 min. The observed increases in extravascular lung water ratios (pulmonary edema), bronchoalveolar lavage, and pleural protein in the saline control group (683 kPa) were not evident with DBcAMP treatment. DBcAMP pretreatment effects were also seen with the white blood cell counts and the percent of neutrophils in the bronchoalveolar lavage. Urinary levels of thromboxane B2, 11-dehydrothromboxane B2, and leukotriene E4 were significantly increased with the 683 kPa saline control decompression exposure. DBcAMP reduced the decompression-induced leukotriene E4 production in the urine. Plasma levels of thromboxane B2, 11-dehydrothromboxane B2, and leukotriene E4 were increased with the 683-kPa exposure groups. DBcAMP treatment did not affect these changes. The 11-dehydrothromboxane B2 and leukotriene E4 levels in the bronchoalveolar lavage were increased with the 683 kPa exposure and were reduced with the DBcAMP treatment. Our results indicate that DBcAMP has the capability to reduce eicosanoid production and limit membrane permeability and subsequent edema formation in rats experiencing decompression sickness.

Animals↗
PubMed1975

Incidence of vestibular symptomatology in 2,500 U.S. Navy diving accidents (1933-1970).

The U.S. Navy diving accident records of 2,500 cases for the years 1933 to 1970 were analyzed and sorted into Type I and Type II decompression sickness. Type II was further sorted into "vestibular" and "other" categories. It was concluded that Type II symptoms accounted for 30% of the decompression accidents and it was estimated that the overall incidence of vestibular symptomatology was between 10 and 20%. Nearly 30% of the Type II cases were diagnosed as having vestibular involvement, although almost 60% of the cases contained a report of a symptom typically associated with the vestibular system complex, e.g., dizziness and nausea.

Accidents↗
PubMed2003

Staged decompression to 3.5 psi using argon-oxygen and 100% oxygen breathing mixtures.

INTRODUCTION: The current extravehicular activity (EVA) space suit at 4.3 psia causes hand and arm fatigue and is too heavy for Martian EVA. A 3.5 psia EVA pressure suit requires increased preoxygenation time but would reduce structural complexity, leak rate, and weight while increasing mobility, comfort, and maintainability. On Mars, nitrogen and argon are available to provide the inert gas necessary for a fire-resistant habitat atmosphere, eliminating need for transport. This study investigated breathing argon/oxygen and 100% oxygen gas mixtures during staged decompression prior to exposure to 3.5 psia. METHOD: During this study, 40 subjects each completed 3 hypobaric exposures to 3.5 psia for 3 h in a reclined position: (A) a 4-h 25-min 14.7-psia (ground level) denitrogenation (100% oxygen breathing) prior to exposure to 3.5 psia; (B) the same as A, utilizing a 7.3-psia stage denitrogenation; and (C) the same as B, with 62% argon-38% oxygen (ARGOX) during the stage. Venous gas emboli (VGE) were monitored with echocardiography. RESULTS: Decompression sickness (DCS) incidence at 3.5 psia with ARGOX at 7.3 psia (C) was significantly higher than with oxygen breathing with or without staged decompression: there was 78% DCS for C compared with 33% and 55% DCS, respectively, for A and B. The corresponding VGE incidences were 73% (C) compared with 33% (A) and 45% (B). CONCLUSION: Preoxygenation at a 7.3-psia stage resulted in a higher DCS risk at 3.5 psia than ground level preoxygenation. It is suggested that an 8.0-psia stage pressure could eliminate this difference. Unfavorable results after preoxygenation with ARGOX indicate argon on-gassing was significant.

Adolescent↗
PubMed2004

A deep stop during decompression from 82 fsw (25 m) significantly reduces bubbles and fast tissue gas tensions.

In spite of many modifications to decompression algorithms, the incidence of decompression sickness (DCS) in scuba divers has changed very little. The success of stage, compared to linear ascents, is well described yet theoretical changes in decompression ratios have diminished the importance of fast tissue gas tensions as critical for bubble generation. The most serious signs and symptoms of DCS involve the spinal cord, with a tissue half time of only 12.5 minutes. It is proposed that present decompression schedules do not permit sufficient gas elimination from such fast tissues, resulting in bubble formation. Further, it is hypothesized that introduction of a deep stop will significantly reduce fast tissue bubble formation and neurological DCS risk. A total of 181 dives were made to 82 fsw (25 m) by 22 volunteers. Two dives of 25 min and 20 min were made, with a 3 hr 30 min surface interval and according to 8 different ascent protocols. Ascent rates of 10, 33 or 60 fsw/min (3, 10, 18 m/min) were combined with no stops or a shallow stop at 20 fsw (6 m) or a deep stop at 50 fsw (15 m) and a shallow at 20 fsw (6 m). The highest bubbles scores (8.78/9.97), using the Spencer Scale (SS) and Extended Spencer Scale (ESS) respectively, were with the slowest ascent rate. This also showed the highest 5 min and 10 min tissue loads of 48% and 75%. The lowest bubble scores (1.79/2.50) were with an ascent rate of 33 fsw (10 m/min) and stops for 5 min at 50 fsw (15 m) and 20 fsw (6 m). This also showed the lowest 5 and 10 min tissue loads at 25% and 52% respectively. Thus, introduction of a deep stop significantly reduced Doppler detected bubbles together with tissue gas tensions in the 5 and 10 min tissues, which has implications for reducing the incidence of neurological DCS in divers.

Atmospheric Pressure↗
PubMedDate not supplied

A simple probabilistic model for standard air dives that is focused on total decompression time.

A statistical fit of an algorithm to "calibration data" gives parameter values for a "probabilistic decompression model." Our objective is to prepare a simple model that will estimate risk of decompression sickness (DCS) in air dives. We develop a logistic regression model using calibration data from carefully controlled experimental dives recorded in the U.S. Navy Decompression Database. We exclude saturation dives, which can have very long decompression times. For most depths, our model's prescriptions for 2% probability of DCS avoid the experimental DCS cases without mandating excessive time at decompression stops. Our model indicates that the long decompression times prescribed by some previous probabilistic models are not necessary. Our model cannot be used operationally because it cannot calculate depths and times at decompression stops; however, there is general concurrence between our model and prescriptions of a deterministic model known as the VVal-18 Algorithm; this supports the adoption of theVVal-18 Algorithm for operational use on decompression dives.

Air↗
PubMed1989

Influence of heliox, oxygen, and N2O-O2 breathing on N2 bubbles in adipose tissue.

Bubbles in rat adipose tissue were studied at 1 bar after decompression from an exposure to air at 3.3 bars (absolute) for 4 h. During air breathing the bubbles grew throughout the observation period. During heliox (80:20) breathing they shrank and eventually disappeared from view. If the breathing gas was changed from heliox back to air or to N2O-O2 (80:20) while the bubbles still had an appreciable size, they started growing again. If the change to N2O was done after or a few minutes before a bubble disappeared from view, it did not reappear. During breathing of 100% O2, most bubbles containing N2 initially grew and then maintained their size for a while before diminishing. However, some bubbles did not start shrinking during the 2-3-h observation period. The relevance of the findings to heliox treatment of CNS decompression sickness after air dives is discussed.

Adipose Tissue↗
PubMed1980

Induced vestibular dysfunction in squirrel monkeys during rapid decompression.

The symptoms of postural instability and dizziness associated with decompression sickness could be ascribed to either damage of the vestibular apparatus or to central nervous system damage. However, a histological study of monkeys exposed to decompression reveals that these symptoms primarily result from damage to the vestibular apparatus (unless there are accompanying central deficits). Furthermore, the damage is of a type that causes new bone growth to occlude the otic fluid spaces of the semicircular canals. In some instances, there is sufficient bone growth to render the cristae ampullares as non-functional end organs. Such diminished vestibular function would present a serious threat to the diver.

Animals↗
PubMed1997

Recompression treatments during the recovery of TWA Flight 800.

After the crash of TWA flight 800, U.S. Navy (USN) and civilian divers recovered the aircraft and the victims' remains from 117 feet of sea water (fsw). Safety information was gathered from observations, interviews, and medical and diving records. Of 752 dives employing surface decompression using oxygen (SDO2), 10 divers required recompression treatments, mainly for type 2 decompression sickness (DCS). When using hot water heating, the DCS risk was high until the dive profiles were modified. Divers made nearly 4,000 no-decompression scuba dives. In eight scuba divers and one tender treated with recompression, the diagnoses included DCS (3), arterial gas embolism (AGE) (1), and vascular headache (2). All USN divers recovered fully. The experience is consistent with previous work suggesting an increase in DCS risk in warmer SDO2 divers. The USN SDO2 tables can be made safer by limiting bottom time and extending decompression. Even under stressful conditions, rapid ascents resulting in AGE are uncommon. Vascular headaches can mimic DCS by responding to oxygen.

Accidents, Aviation↗
PubMedDate not supplied

Dysbaric osteonecrosis. Etiological and pathogenetic concepts.

Dysbaric osteonecrosis appears to be independent of decompression sickness. The 2 conditions, however, may share etiologic and pathogenetic factors. The incidence of osteonecrosis is influenced by the number of hyperbaric exposures, extent of pressure, decompression profile and possibly by the rate of compression and degree of obesity. Though etiology and pathogenesis are unclear, osteonecrosis is probably due to ischemia, with gas bubbles causing direct or indirect circulatory impairment. In vitro experiments, as well as human and animal studies, suggest multiple pathogenetic mechanisms: intraosseous vessel compression by extravascular bubbles; vessel obstruction by bubbles, fibrin thrombi, platelet aggregates, clumped erythrocytes or coalesced lipids; and narrowing of arterial lumina by bubble-induced myointimal thickening. Obstructing materials, whether autochthonous or embolic, may result from blood-bubble interface reactions. Rheologic changes and blood flow redistribution could play contributing roles. It seems likely that multiple pathogenetic factors act in concert or sequentially. Proposed nonischemic changes, such as hyperoxic injury gas-induced osmosis, or autoimmunity, lack sufficient supporting evidence. The peculiar vulnerability of bone may be related to gas supersaturation of the fatty marrow; sensitivity to extravascular gas pressure because of tissue rigidity; poor vascularization; and the presence of uranium 238 which promotes nucleation and subsequent gas bubble formation.

Animals↗
PubMed2003

Negative pressure breathing enhances nitrogen elimination.

BACKGROUND: The rate of nitrogen elimination during decompression is primarily dependent on tissue perfusion and, therefore, cardiac output (CO). Negative pressure breathing (NPB) is thought to increase CO by enhancing venous return and, consequently, the rate of nitrogen elimination. This notion was investigated in the present study. METHODS: Nitrogen elimination was measured in five subjects lying supine while breathing a nitrogen free gas (79% Ar, 20% O2) supplied at -15 cm H2O (-1.5 kPa) or at atmospheric pressure. RESULTS: Over a 2-h washout period, NPB increased nitrogen elimination by 39.2 +/- 21.7% (mean +/- SD), increased calf blood flow by 34.1 +/- 34.6%, and elevated BP slightly during the last half of the experiment. Negative pressure breathing did not significantly change CO; the increase in nitrogen elimination may have been due to redistribution of blood flow. CONCLUSIONS: Negative pressure breathing appears to be a useful means of increasing nitrogen elimination and should be considered in situations such as decompression or treatment of decompression sickness where this effect may be beneficial.

Administration, Inhalation↗
PubMedDate not supplied

Effect of He-O2, O2, and N2O-O2 breathing on injected bubbles in spinal white matter.

Injected air bubbles in spinal white matter in the rat were studied at 1 bar after decompression from an exposure to air at 3.1 bar (absolute) for 4 h. During air breathing all injected bubbles grew for the first 2 h of the observation period. Thereafter three of nine bubbles began to shrink and one of them disappeared. During breathing of heliox (80:20) bubbles consistently shrank and disappeared from view. If the breathing gas was changed from heliox to N2O-O2 (80:20), while bubbles still had an appreciable size, they started growing again. If the change to N2O-O2 was done after a bubble disappeared from view, it did not reappear. During breathing of 100% oxygen, all bubbles initially grew. Subsequently they all shrank and disappeared at about the same time after gas shift, as during heliox breathing. The effect of heliox treatment on CNS decompression sickness after air dives is discussed.

Adipose Tissue↗
PubMed1985

Analyses of variables underlying U.S. Navy diving accidents.

U.S. Navy diving logs were examined to determine the most frequently occurring diving accidents and to identify significant underlying factors. Of the 1174 incidents reported during the course of 706,259 dives, decompression sickness and barotraumas were the most prevalent. Mishap incidence increased significantly with dive depth. Dives for selection or experimental purposes, as well as saturation diving and surface decompressions among decompression schedule types, were at an elevated risk of terminating in an accident. Older divers were disproportionately assigned to deep dives. Eighty-one percent of diving mishaps ended in complete relief for the diver while 18% terminated in substantial relief.

Accidents, Occupational↗
PubMed1982

Aseptic necrosis in compressed air tunnel workers using current OSHA decompression schedules.

Aseptic necrosis (dysbaric osteonecrosis) was discovered in two compressed air tunnel workers who had used the present Occupational Health and Safety Administration (OSHA) decompression tables for compressed air tunneling at pressures greater than 36 pounds per square inch gauge (psig). A roentgenographic study was made of 21 men who had worked at pressures up to 43 psig using the OSHA schedules. Bone scanning was also included. Seven of the men (33%) were found to have aseptic necrosis involving the shoulders, hips or distal femoral shafts and proximal tibia. It became evident that the present OSHA schedules caused not only an unacceptable incidence of decompression sickness but also aseptic necrosis at pressures over 36 psig. New interim tables that are more conservative and that use either air or oxygen as a breathing gas during decompression are undergoing laboratory and worksite evaluation.

Adult↗
PubMed2005

Evidence for increasing patency of the foramen ovale in divers.

Using a standardized contrast-enhanced transesophageal echocardiographic technique, a group of divers was reexamined for the presence and size of patent foramen ovale (PFO) 7 years after their initial examinations. Unexpected but significant increases in the prevalence and size of PFO were found, suggesting a possible increasing risk for decompression sickness in these divers over time.

Decompression Sickness↗
PubMedDate not supplied

Fatty acid composition of plasma lipids and erythrocyte membranes during simulated extravehicular activity.

Ten subjects (from 27 to 41 years) have been participated in 32 experiments. They were decompressed from ground level to 40-35 kPa in altitude chamber when breathed 100% oxygen by mask and performed repeated cycles of exercises (3.0 Kcal/min). The intervals between decompressions were 3-5 days. Plasma lipid and erythrocyte membrane fatty acid composition was evaluated in the fasting venous blood before and immediately after hypobaric exposure. There were 7 cases decompression sickness (DCS). Venous gas bubbles (GB) were detected in 27 cases (84.4%). Any significant changes in the fatty acid composition of erythrocyte membranes and plasma didn't practically induce after the first decompression. However, by the beginning of the second decompression the total lipid level in erythrocyte membranes decreased from 54.6 mg% to 40.4 mg% in group with DCS symptoms and from 51.2 mg% to 35.2 mg% (p<0.05) without DCS symptoms. In group with DCS symptoms a tendency to increased level of saturated fatty acids in erythrocyte membranes (16:0, 18:0), the level of the polyunsaturated linoleic fatty acid (18:2) and arachidonic acid (20:4) tended to be decreased by the beginning of the second decompression. Insignificant changes in blood plasma fatty acid composition was observed in both groups. The obtained biochemical data that indicated the simulated extravehicular activity (EVA) condition is accompanied by the certain changes in the blood lipid metabolism, structural and functional state of erythrocyte membranes, which are reversible. The most pronounced changes are found in subjects with DCS symptoms.

Adult↗