Evaluating the risk of decompression sickness for a yo-yo dive using a rat model.

PURPOSE: The frequent ascents made during yo-yo diving may contribute to gas bubble clearance but paradoxically may also increase the risk of central nervous system decompression illness (DCI). We evaluated the risk of DCI due to yo-yo dives with very short surface intervals, using a controlled animal model. METHODS: Dives were conducted on air to a depth of 90 meters (10 atmospheres absolute) for 32 minutes of bottom time, at a descent/ascent rate of 10 meters/ minute. Sprague-Dawley rats weighing ~ 300 grams were divided randomly into three groups. Group A performed a square dive protocol without any surface intervals, Group B conducted a protocol that included two surface intervals during the dive, and Group C performed a protocol with three surface intervals. Ascent/descent rate for surface intervals, each lasting one minute, was also 10 meters/minute. RESULTS: Manifestations of DCI were observed in 13 of 16 animals in Group A (81.3%), six of 12 in Group B (58.3%), and two of 12 in Group C (16.7%). Mortality rates were similar in all groups. CONCLUSIONS: Surface intervals during dives breathing air significantly reduced DCI risk in the rat. Further studies are required using a larger animal model to reinforce the results of the present investigation.

Evidence for the initiation of decompression sickness by exposure to intense underwater sound.

Mass stranding of cetaceans (whales and dolphins), in close association with the activity of naval sonar systems, has been reported on numerous occasions. Necropsy showed bubble-associated lesions similar to those described in human decompression sickness (DCS). We examined the hypothesis that exposure to underwater sound may potentiate DCS. Rats were subjected to immersion and simulated dives with and without simultaneous acoustic transmissions at pressure levels and frequencies of 204 dB/8 kHz and 183.3 dB/15 kHz. DCS severity was assessed using the rotating wheel method. Recording of somatosensory evoked potentials (SSEPs) was employed under general anesthesia as an electrophysiological measure of neurologic insult. A significantly higher rate of decompression sickness was found among animals exposed to the 204-dB/8-kHz sound field. Significantly higher pathological SSEPs scores were noted for both underwater sound protocols. Pathological SSEPs scores in animals immersed during the acoustic transmissions, but without changes in ambient pressure, were comparable to those observed in animals exposed to the dive profile. The results demonstrate induction of neurological damage by intense underwater sound during immersion, with a further deleterious effect when this was combined with decompression stress. The study outcome has potential implications for human diving safety and may provide an explanation for the mass stranding of cetaceans purportedly associated with sonar activity.

Methylphenidate and the risk of acute central nervous system oxygen toxicity: a rodent model and observational data in human divers.

Introduction: The effects of methylphenidate, a stimulant often prescribed for the treatment of attention-deficit/hyperactivity disorder (ADHD), on the development of central nervous system oxygen toxicity (COT) have not been experimentally evaluated. Methods: The records of all pure-oxygen-rebreather divers evaluated at our institution from 1975-2022 were assessed. Cases of COT were defined as a new onset of tinnitus, tunnel vision, myoclonus, headache, nausea, loss of consciousness, or seizures resolving within 15 minutes from breathing normobaric air, and matched 4:1 with similar controls. Any medications issued to the diver in the preceding three months, including methylphenidate, were recorded. In the animal arm of this study, male mice were exposed to increasing doses of methylphenidate orally, with subsequent exposure to hyperbaric O2 until clinically evident seizures were recorded. Results: Seventy-five cases of COT were identified in divers, occurring at a median of 80 (range 2-240) minutes after dive initiation at a median depth of 5 m (2-13). Hypercarbia was documented in 11 (14.7%) cases. Prescription of methylphenidate in the preceding three months was not associated with increased risk (OR 0.72, 95% CI 0.16-3.32) of COT. In mice, increasing methylphenidate exposure dose was associated with significantly longer mean COT latency time being 877 s (95% CI 711-1,043) with doses of 0 mg·kg⁻¹; 1,312 s (95% CI 850-1,773) when given 0.75 mg·kg⁻¹; and 1,500 s (95% CI 988-2,012) with 5 mg·kg⁻¹ (F = 4.635, P = 0.014). Conclusions: Observational human data did not demonstrate an association between methylphenidate and an increased risk of COT. Methylphenidate exposure in mice prolongs COT latency and may have protective effects against COT.

Exposure to hyperbaric O2 levels leads to blood-brain barrier breakdown in rodents.

INTRODUCTION: Hyperbaric oxygen has been used as a medical treatment tool in hyperbaric chambers and is an integral part of professional and combat divers' activity. In extreme cases, exposure to hyperbaric oxygen can develop central nervous system oxygen toxicity (CNS-OT), which leads to seizures and eventually death. CNS-OT is caused by neuronal hyperactivity due to high oxygen levels, potentially damaging brain cells including the blood-brain barrier (BBB). However, the effect of hyperbaric oxygen levels on the healthy BBB has not been characterized directly yet. METHODS: Six or three different groups of ~ eight rats or mice, respectively, were exposed to increasing levels of partial pressure of oxygen (0.21 to 5 ATA) in a hyperbaric chamber, followed by MRI scanning with gadolinium. Statistical significance (adjusted p-value ≤ 0.05) was assessed using linear regression and ordinary one-way (rats) or two-way (mice) ANOVA with correction of multiple comparison tests. In rats, the effect of 100% oxygen at 5 ATA was independently validated using FITC-Dextran (5 kDa). Statistical significance (p-value ≤ 0.05) was assessed using Welch's t-test and effect size was calculated by Cohen's D. RESULTS: In rats, analyzed MRI scans showed a significant trend of increase in the % gadolinium in brain tissues as a result of hyperbaric oxygen pressures (p-value = 0.0079). The most significant increase was measured at 4 ATA compared to air (adjusted p-value = 0.0461). Significant increased FITC-Dextran levels were measured in the rats' brains under 100% oxygen at 5 ATA versus air (p-value = 0.0327; Effect size = 2.0). In mice, a significant increase in gadolinium penetration into the hippocampus and frontal cortex was measured over time (adjusted p-value < 0.05) under 100% oxygen at 3 and 5 ATA versus air, and between the treatments (adjusted p-value < 0.0001). CONCLUSIONS: The BBB is increasingly disrupted due to higher levels of hyperbaric oxygen in rodents, indicating a direct relation between hyperbaric oxygen and BBB dysregulation for the first time. We suggest considering this risk in different diving activities, and protocols using a hyperbaric chamber. On the other hand, this study highlights the potential therapeutic usage of hyperbaric oxygen for controlled drug delivery through the BBB into brain tissues in different brain-related diseases.

Use of a fast transcutaneous CO2 detector to evaluate escape hoods: the "CAPS 2000" with the inlet valves removed from the nose-cup as a test case.

INTRODUCTION: The traditional method used to evaluate escape masks has been to examine the composition of the inspired gas, although arterial carbon dioxide (CO2) and oxygen (O2) would be more relevant physiological parameters. The recent development of reliable, fast-responding transcutaneous CO2 detectors makes it possible to evaluate arterial CO2 and O2 saturation. The CAPS 2000 escape mask was designed to protect the head and respiratory system from chemical or biological attack. The question arises of whether there might be a risk of dangerous hypoxia-hypercapnia in rebreathing from the mask because of leakage of the expired gas from the nose-cup into the hood, although theoretical considerations rule this out. We studied a worst case scenario. METHODS: Nine subjects wore the CAPS 2000 for 15 minutes after removal of the inspiratory valves. A mass spectrometer and transcutaneous sensor were used to measure O2 and CO2, arterial O2 saturation, and arterial partial pressure of CO2 (PCO2). RESULTS: Blood oxygen saturation decreased from an initial value of 98.4% to 96.2% at 2 minutes, subsequently rising and stabilizing at a level similar to control. Subcutaneous PCO2 rose from the control level of 36 to 43 torr after 5 minutes, then decreased to 42 torr and stabilized at that level. Inspired PO2 dropped from 21% to 16% at 3 to 4 minutes, rose to 17% at 8 minutes, and stabilized thereafter. Inspired PCO2 rose to 3% in the first minute and continued to rise to 3.5% at 3 minutes, after which it slowly decreased to 3% and stabilized at that level. DISCUSSION: The transcutaneous CO2 detector provided a true indication of the physiological state of the subject, and these parameters are sufficient on their own for the evaluation of breathing masks. CO2 and O2 did not reach dangerous levels with the inspiratory valves removed from the CAPS 2000 mask.

Flow resistance, work of breathing of humidifiers, and endotracheal tubes in the hyperbaric chamber.

Humidification of inspired gas is critical in ventilated patients, usually achieved by heat and moisture exchange devices (HMEs). HME and the endotracheal tube (ETT) add airflow resistance. Ventilated patients are sometimes treated in hyperbaric chambers. Increased gas density may increase total airway resistance, peak pressures (PPs), and mechanical work of breathing (WOB). We tested the added WOB imposed by HMEs and various sizes of ETT under hyperbaric conditions. We mechanically ventilated 4 types of HMEs and 3 ETTs at 6 minute ventilation volumes (7-19.5 L/min) in a hyperbaric chamber at pressures of 1 to 6 atmospheres absolute (ATA). Peak pressure increased with increasing chamber pressure with an HME alone, from 2 cm H2O at 1 ATA to 6 cm H(2)O at 6 ATA. Work of breathing was low at 1 ATA (0.2 J/L) and increased to 1.2 J/L at 6 ATA at minute ventilation = 19.5 L/min. Connecting the HME to an ETT increased PP as a function of peak flow and chamber pressure. Reduction of the ETT diameter (9 > 8 > 7.5 mm) and increase in chamber pressure increased the PP up to 27.7 cm H2O, resistance to 33.2 cmH2O*s/L, and WOB to 3.76 J/L at 6 ATA with a 7.5-mm EET. These are much greater than the usually accepted critical peak pressures of 25 cm H2O and WOB of 1.5 to 2.0 J/L. Endotracheal tubes less than 8 mm produce significant added WOB and airway pressure swings under hyperbaric conditions. The hyperbaric critical care clinician is advised to use the largest possible ETT. The tested HMEs add negligible resistance and WOB in the chamber.

Oxygen pretreatment as protection against decompression sickness in rats: pressure and time necessary for hypothesized denucleation and renucleation.

Pretreatment with HBO at 300-500 kPa for 20 min reduced the incidence of decompression sickness (DCS) in a rat model. We investigated whether this procedure would be effective with lower oxygen pressures and shorter exposure, and tried to determine how long the pretreatment would remain effective. Rats were pretreated with oxygen at 101 or 203 kPa for 20 min and 304 kPa for 5 or 10 min. After pretreatment, the animals were exposed to air at 1,013 kPa for 33 min followed by fast decompression. Pretreatment at 101 or 203 kPa for 20 min and 304 kPa for 10 min significantly reduced the number of rats with DCS to 45%, compared with 65% in the control group. However, after pretreatment at 304 kPa for 5 min, 65% of rats suffered DCS. When pretreatment at 304 kPa for 20 min was followed by 2 h in normobaric air before compression and decompression, the outcome was worse, with 70-90% of the animals suffering DCS. This is probably due to the activation of "dormant" micronuclei. The risk of DCS remained lower (43%) when pretreatment with 100% O(2) at normobaric pressure for 20 min was followed by a 2 h interval in normobaric air (but not 6 or 24 h) before the hyperbaric exposure. The loss of effectiveness after a 6 or 24 h interval in normobaric air is related to micronuclei rejuvenation. Although pretreatment with hyperbaric O(2) may have an advantage over normobaric hyperoxia, decompression should not intervene between pretreatment and the dive.

Symptoms of central nervous system oxygen toxicity during 100% oxygen breathing at normobaric pressure with increasing inspired levels of carbon dioxide: a case report.

The greatest danger faced by divers who use oxygen-enriched gas mixtures is central nervous system oxygen toxicity (CNS-OT). CNS-OT is characterised by convulsions resembling grand-mal epileptic seizures, which may terminate in drowning and death. Elevated arterial levels of carbon dioxide (CO2) (hypercapnia) represent a major risk factor for CNS-OT when breathing hyperoxic gas mixtures. To reduce the risk of a diver being involved in a CNS-OT incident due to hypercapnia, candidates for combat diving are examined at our institute using a routine physiological training procedure, in which they are tested for CO2 detection and retention. We present the case of a candidate for combat diving, who unexpectedly exhibited signs typical of CNS-OT while breathing pure oxygen under normobaric conditions with > 3 kPa inspired CO2. Severe headache and nausea, as well as facial muscle twitching, appeared during one of these routine tests. Subsequent medical examination including neurological tests, magnetic resonance imaging and an electroencephalogram were unremarkable. To the best of our knowledge, an event such as this has never previously been published in the medical literature. We present a discussion of the case, and a review of the relevant literature regarding CO2 as a risk factor for the development of CNS-OT.

Personal CO2 scrubbing device for use in a disabled submarine.

INTRODUCTION: In the sunken submarine, a breakdown in the power supply can disrupt the provision of fresh air and the absorption of CO2. A personal device based on a breathing mask and the soda lime canisters used in the submarine is proposed for CO2 absorption. METHODS: In an unmanned experiment, a breathing simulator provided a flow of air at 8.7 L x min(-1) and a carbon dioxide output of 20.9 L x h(-1), which passed through either one or two 3.8-kg canisters of soda lime. In the manned experiment, four subjects wore the breathing mask, which was connected to two 3.8-kg canisters of soda lime placed in a bag, and remained for 24 h in a sealed hyperbaric chamber. They inspired the chamber atmosphere and expired via the canisters. RESULTS: In the unmanned experiment, the concentration of CO2 when a single canister was used reached 1% after 8 h, 2% after 22 h, and 2.5% after 37 h. With two canisters connected in sequence, the concentration of CO2 reached 1% after 48 h, while the pressure at the entrance to the canisters did not exceed 0.7 cm H2O. In the manned experiment, the CO2 concentration decreased over the first 12 h from its initial value of 1.3%, stabilizing during sleep at 0.75%. DISCUSSION: The personal carbon dioxide absorption device lowered the ambient CO2 level over a period of 24 h, and could maintain this level for a further 24 h. Keeping CO2 at a low level has an advantage over the peaks of 3% obtained with absorbent LiOH curtains, where elevated pressure and increased P(CO2) may have an adverse effect on the survivors. Some of the crew can remain active without using the device, while the others do the job of clearing the carbon dioxide for the whole crew.

Evaluating the thermal protection provided by a 2‒3 mm wet suit during fin diving in shallow water with a temperature of 16‒20°C.

INTRODUCTION: The purpose of the study was to evaluate the thermal protection provided by a 2-3 mm surfing wet suit during at least two hours of fin diving in shallow water with a temperature of 16-20°C. We examined the effect of wearing the suit while diving in cold water on cognitive performance, muscle strength, and hand motor function. METHODS: Subjects were six male well-trained rebreather divers, 19-23 years old, acclimatised to cold. They attended the laboratory on three separate occasions, when we conducted the experiment at one of three temperatures, 16, 18, and 20°C. Core temperature (gastrointestinal system), skin temperature, oxygen consumption, and cold perception were evaluated during the test. Before and immediately after the dives, subjects performed a series of cognitive, manual dexterity, and muscle strength tests. RESULTS: Core temperature decreased by 0.35-0.81°C over the two hours at all three water temperatures. No subject reached a core temperature below 35°C. The decrease in upper body skin temperature during the two hour dive ranged between 5.97 and 8.41°C (P < 0.05). Two hours diving in 16-20°C water resulted in a significant increase in the time taken to perform the task of unlinking and reassembling four shackles (∼30% longer, P < 0.05). No effect was found on the cognitive or muscle strength tests. CONCLUSIONS: A 2-3 mm wet suit provides adequate thermal protection in trained and cold-acclimatised young males engaged in active diving in shallow water with a temperature of 16°C and above.

The Effect of Aging on the Ventilatory Response to Wearing a Chemical, Biological, Radiological, and Nuclear Hood Respirator at Rest and During Mild Exercise.

BACKGROUND: Structural changes in the human body resulting from aging may affect the response to altered levels of O2 and CO2. An abnormal ventilatory response to a buildup of CO2 in the inspired air due to rebreathing may result in adverse effects, which will impair the individual's ability to function under stress. The purpose of this study was to evaluate the effect of age on the respiratory response to wearing an escape hood at rest and during mild exercise. METHODS: Subjects were seven healthy, young adult males (20-30 years) and seven healthy, middle-aged males (45-65 years). Inspired CO2 and O2, breathing pattern (tidal volume [VT] and breathing frequency [F]), and mouth inspiratory and expiratory pressures, were measured at rest and during mild exercise (50 w) while wearing the CAPS 2000 escape hood (Shalon Chemical Industries and Supergum-Rubber and Plastic Technology, Tel Aviv, Israel). FINDINGS: Resting inspired CO2 was higher in the middle-aged group compared with the young group (2.25% ± 0.42% and 1.80% ± 0.34%, respectively; p < 0.05). Breathing pattern in the middle-aged group tended to be shallower and faster compared with the young group (VT: 0.69 ± 0.27 L and 0.79 ± 0.32 L, respectively; F: 14.7 ± 4.0 breaths/min and 12.4 ± 2.8 breaths/min, respectively). During exercise, there was a trend toward a high inspired CO2 in the middle-aged group compared with the young group (2.18% ± 0.40% CO2 and 1.94% ± 0.70% CO2, respectively). A correlation was found between age and inspired CO2 when wearing the escape hood (r2 = 0.375; p < 0.05). DISCUSSION: The age-related decrease in pulmonary function, together with the finding in this study of a higher inspired CO2 in middle-aged subjects wearing the CAPS 2000, may represent a greater risk for persons of middle age wearing an escape hood. RECOMMENDATIONS: On the basis of this study, it would appear reasonable to recommend that new respirators be evaluated on subjects from different age groups, to ensure the safety of both young and old.

The transition from day-to-night activity is a risk factor for the development of CNS oxygen toxicity in the diurnal fat sand rat (Psammomys obesus).

Performance and safety are impaired in employees engaged in shift work. Combat divers who use closed-circuit oxygen diving apparatus undergo part of their training during the night hours. The greatest risk involved in diving with such apparatus is the development of central nervous system oxygen toxicity (CNS-OT). We investigated whether the switch from day-to-night activity may be a risk factor for the development of CNS-OT using a diurnal animal model, the fat sand rat (Psammomys obesus). Animals were kept on a 12:12 light-dark schedule (6 a.m. to 6 p.m. at 500 lx). The study included two groups: (1) Control group: animals were kept awake and active during the day, between 09:00 and 15:00. (2) Experimental group: animals were kept awake and active during the night, between 21:00 and 03:00, when they were exposed to dim light in order to simulate the conditions prevalent during combat diver training. This continued for a period of 3 weeks, 5 days a week. On completion of this phase, 6-sulphatoxymelatonin (6-SMT) levels in urine were determined over a period of 24 h. Animals were then exposed to hyperbaric oxygen (HBO). To investigate the effect of acute melatonin administration, melatonin (50 mg/kg) or its vehicle was administered to the animals in both groups 20 min prior to HBO exposure. After the exposure, the activity of superoxide dismutase, catalase and glutathione peroxidase was measured, as were the levels of neuronal nitric oxide synthase (nNOS) and overall nitrotyrosylation in the cortex and hippocampus. Latency to CNS-OT was significantly reduced after the transition from day-to-night activity. This was associated with alterations in the level of melatonin metabolites secreted in the urine. Acute melatonin administration had no effect on latency to CNS-OT in either of the groups. Nevertheless, the activity of superoxide dismutase and catalase, as well as nitrotyrosine and nNOS levels, were altered in the hippocampus following melatonin administration. On the basis of these results, we suggest that a switch from diurnal to nocturnal activity may represent an additional risk factor for the development of CNS-OT. Utilizing a diurnal animal model may contribute to our understanding of the heightened risk of developing CNS-OT when diving with closed-circuit oxygen apparatus at night.

Acute tobacco smoke exposure promotes mitochondrial permeability transition in rat heart.

Chronic exposure to tobacco smoke is known to impair mitochondrial function. However, the effect of acute tobacco smoke exposure (ATSE) in vivo, as might occur in social settings, on mitochondrial function and calcium handling of cardiac cells has not been examined. It was hypothesized that ATSE might adversely modify mitochondrial function as reflected in mitochondrial energetics, membrane potential, and calcium transport. Mitochondria were isolated from the hearts of adult rats either exposed to 6 h of environmental tobacco smoke ( approximately 60 mg/mm3 tobacco smoke particles) or sham exposure. To model a calcium stress similar to ischemia/reperfusion, mitochondria were exposed to a Ca2+ bolus with measurement of membrane potential, energetics, Ca2+uptake and release, and redox state. ATSE mitochondria were characterized by significantly higher ADP-stimulated ATP production and a more reduced redox state (NADH ratio) under basal conditions without observed changes in resting Psim. Exposure of ATSE mitochondria to Ca2+stress resulted in significantly more rapid depolarization of Psim. The initial rate of Ca2+uptake was not altered in ATSE mitochondria, but CsA-sensitive Ca2+ release was significantly increased. ATSE does not significantly alter resting mitochondrial function. However, ATSE modifies the response of cardiac mitochondria to calcium stress, resulting in a more rapid depolarization and subsequent release of Ca2+ via the mitochondrial permeability transition (MPT).

Evidence for the infiltration of gas bubbles into the arterial circulation and neuronal injury following "yo-yo" dives in pigs.

"Yo-yo" diving may place divers at a greater risk of neurologic decompression illness (DCI). Using a rat model, we previously demonstrated that "yo-yo" diving has a protective effect against DCI. In the current study, we evaluated the risk of neurologic DCI following "yo-yo" dives in a pig model. Pigs were divided into four groups. The Control group (group A) made a square dive, without excursions to the surface ("peeps"). Group B performed two "peeps," group C performed four "peeps," and group D did not dive at all. All dives were conducted on air to 5 atm absolute, for 30-min bottom time. Echocardiography was performed to detect cardiac gas bubbles before the dive, immediately after, and at 90-min postdive. Motor performance was observed during the 5-h postdive period. Symptoms increased dramatically following a dive with four "peeps." Gas bubbles were detected in the right ventricle of all animals except for the sham group and in the left ventricle only after the four-peep dive. Neuronal cell injury was found in the spinal cord in each of the three experimental groups, tending to decrease with an increase in the number of "peeps." A four-peep "yo-yo" dive significantly increased the risk of neurologic DCI in pigs. Following a four-peep dive, we detected a higher incidence of bubbles in the left ventricle, supporting the common concern regarding an increased risk of neurologic DCI, albeit there was no direct correlation with the frequency of "red neurons" in the spinal cord.

Alteration of blood glucose levels in the rat following exposure to hyperbaric oxygen.

Findings regarding blood glucose level (BGL) on exposure to hyperbaric oxygen (HBO) are contradictory. We investigated the influence of HBO on BGL, and of BGL on latency to central nervous system oxygen toxicity (CNS-OT). The study was conducted on five groups of rats: Group 1, exposure to oxygen at 2.5 atmospheres absolute (ATA), 90 min/day for 7 days; Group 2, exposure to oxygen once a week from 2 to 6 ATA in increments of 1 ATA/wk, for a period of time calculated as 60% of the latency to CNS-OT (no convulsions); Group 3, exposure to 6 ATA breathing a gas mixture with a pO2 of 0.21; Group 4, received 10 U/kg insulin to induce hypoglycemia before exposure to HBO; Group 5, received 33% glucose to induce hyperglycemia before exposure to HBO. Blood samples were drawn before and after exposures for measurement of BGL. No change was observed in BGL after exposure to oxygen at 2.5 ATA, 90 min/day for 7 days. BGL was significantly elevated after exposure to oxygen at 6 ATA until the appearance of convulsions, and following exposure to 4, 5, and 6 ATA without convulsions (P < 0.01). No change was observed in BGL after exposure to 6 ATA breathing a gas mixture with a pO2 of 0.21. Hypoglycemia shortened latency to CNS oxygen toxicity, whereas hyperglycemia had no effect. Our results demonstrate an influence of HBO exposure on elevation of BGL, starting at 4 ATA. This implies that BGL may serve as a marker for the generation of CNS-OT.

Hyperbaric oxygen may reduce gas bubbles in decompressed prawns by eliminating gas nuclei.

It is accepted that gas bubbles grow from preexisting gas nuclei in tissue. The possibility of eliminating gas nuclei may be of benefit in preventing decompression sickness. In the present study, we examined the hypothesis that hyperbaric oxygen may replace the resident gas in the nuclei with oxygen and, because of its metabolic role, eliminate the nuclei themselves. After pretreatment with oxygen, prawns were 98% saturated with nitrogen before explosive decompression at 30 m/min. Ten transparent prawns were exposed to four experimental profiles in a crossover design: 1) 10-min compression to 203 kPa with air; 2) 10-min compression with oxygen; 3) 10-min compression with oxygen to 203 kPa followed by 12 min air at 203 kPa; and 4) 10 min in normobaric oxygen followed by compression to 203 kPa with air. Bubbles were measured after explosive decompression. We found that pretreatment with hyperbaric oxygen (profile C) significantly reduces the number of bubbles and bubble volume. We suggest that hyperbaric oxygen eliminates bubble nuclei in the prawn.

Heat acclimation prolongs the time to central nervous system oxygen toxicity in the rat. Possible involvement of HSP72.

Oxygen toxicity of the central nervous system (CNS-OT) can occur during diving with oxygen-enriched gas mixtures, or during hyperbaric medical treatment. CNS-OT is characterised by convulsions and sudden loss of consciousness, which may be fatal in diving. Heat acclimation is known to provide cross-tolerance to various forms of stress in different organs, including the brain. We hypothesised that heat acclimation may delay the onset of CNS-OT in the rat. Male Sprague-Dawley rats were acclimated to an ambient temperature of 32 degrees C for 4 weeks. Rats in the control group were kept at 24 degrees C. Both groups were exposed to oxygen at 608 kPa. EEG was recorded continuously until the appearance of the first electrical discharge preceding clinical convulsions. CO(2) production was measured simultaneously with the EEG. Latency to CNS-OT was measured and brain samples were taken for evaluation of heat shock protein 72 (HSP72) levels by Western blot analysis at the end of the acclimation period and during 4 weeks of deacclimation. Latency to CNS-OT was twice as long in the heat-acclimated rat, with insignificant changes in CO(2) production. This prolongation continued for 2 weeks during deacclimation. There was a significant increase in the level of HSP72 following heat acclimation, with a subsequent decrease during deacclimation. We conclude that heat acclimation prolongs latency to CNS-OT in a way that does not involve changes in metabolic rate. During deacclimation there was a linear relationship between latency to CNS oxygen toxicity and the level of HSP72. A possible beneficial effect of HSP72 is discussed.

High-frequency sound transmissions under water and risk of decompression sickness.

We tested the possible occurrence of a neurological insult secondary to high-frequency sound exposure. Immersed, anesthetized rats were subjected to a simulated diving profile designed to induce decompression sickness, while exposed to the transmission of an acoustic beacon. Intermittent sound at a pressure level of 184.5 dB re 1 microPa at 1 m (1.7 kPa), a frequency of 37 kHz, and with a duration of 4 ms, was transmitted in a duty cycle of 0.26%. Four groups, each containing nine animals, were included in the study as follows: group 1, immersion only, no sound exposure; group 2, immersion with sound exposure; group 3, diving simulation when immersed, no sound exposure; group 4, diving simulation when immersed, with sound exposure. Somatosensory evoked potentials (SSEPs) were recorded the day before the study, and a second recording was made 30 min after immersion. Some of the SSEP components disappeared after the dive in 3 rats from group 3 and 2 rats from group 4. SSEP components could not be identified in a significantly larger number of animals from groups 3 and 4, compared with groups 1 and 2. No differences were found in wave latency, amplitude or conduction time. Our data show that the high-frequency sound exposure employed did not contribute to the development of the neurological insult.

High-frequency sound field and bubble formation in a rat decompression model.

High-frequency sound might cause bubble enlargement by rectified diffusion. The purpose of the present study was to investigate gas bubble formation in the immersed diving animal during exposure to high-frequency sound. Anaesthetised rats were subjected to a simulated diving profile while immersed inside a hyperbaric chamber. An acoustic beacon (pinger) was placed ventral to the animal's abdomen, transmitting at an intensity of 208.9 dB re 1 micro Pa and a frequency of 37 kHz. Six groups of eight animals were included in the study as in Table 1, breathing air (n = 4) or Nitrox 72/28 (n = 2), at a depth of 0 m, 30 m or 40 m. Immediately after decompression, the intestinal mesenterium was imaged, and frames were acquired digitally. The number of bubbles and their radii were analysed and compared among the groups. The mean bubble density for group 1 was 1.35 +/- 0.18 bubbles/mm(2), significantly higher when compared with the other groups (p < 0.0001). The average bubble radius for groups 1 and 2 was similar (12.57 +/- 4.1 and 10.63 +/- 1.8 microm, respectively), but significantly larger than in the other groups (p < 0.0002). The percentage of bubbles with a radius greater than 50 microm was significantly higher in group 1 (p < 0.0001). The results suggest that commercially available underwater pingers might enhance bubble growth during deep air diving.

Hyperoxia may reduce energetic efficiency in the trained rat.

BACKGROUND: Several studies have been conducted in recent years in the attempt to improve running performance by the use of hyperbaric oxygen, but there is disagreement as to whether this has any beneficial effect. The purpose of this study was to measure the effect of 24 h breathing 100% O2 in normobaric conditions on energetic efficiency in the trained rat. METHODS: Experiments were carried out on trained rats whose oxygen consumption was evaluated during the training period and on its completion. At the end of the training period, the rats were divided into two groups: 1) rats exposed to air (21% O2) in normobaric conditions; and 2) rats exposed to 100% O2 in normobaric conditions. In addition, two groups of sedentary rats were used: 3) sedentary rats exposed to air (21% O2) in normobaric conditions; and 4) sedentary rats exposed to 100% O2 in normobaric conditions. Energetic efficiency was estimated by measuring O2 consumption at submaximal exercise (45 m.min-1, 10 degrees incline). RESULTS: Training alone reduced O2 consumption by 18% during submaximal exercise. Exposure to 100% oxygen for 24 h in normobaric conditions reversed the effect of complete training by elevating the O2 consumption by 17%, which was close to the oxygen consumption of the rats during the incomplete training period. CONCLUSIONS: Our results suggest that prolonged exposure to hyperoxia induces a reduction in the energetic efficiency of the trained rat. The relevance of these findings to sports and diving is discussed.