Variability in venous gas emboli following the same dive at 3,658 meters.

Exposure to a reduction in ambient pressure such as in high-altitude climbing, flying in aircrafts, and decompression from underwater diving results in circulating vascular gas bubbles (i.e., venous gas emboli [VGE]). Incidence and severity of VGE, in part, can objectively quantify decompression stress and risk of decompression sickness (DCS) which is typically mitigated by adherence to decompression schedules. However, dives conducted at altitude challenge recommendations for decompression schedules which are limited to exposures of 10,000 feet in the U.S. Navy Diving Manual (Rev. 7). Therefore, in an ancillary analysis within a larger study, we assessed the evolution of VGE for two hours post-dive using echocardiography following simulated altitude dives at 12,000 feet. Ten divers completed two dives to 66 fsw (equivalent to 110 fsw at sea level by the Cross correction method) for 30 minutes in a hyperbaric chamber. All dives were completed following a 60-minute exposure at 12,000 feet. Following the dive, the chamber was decompressed back to altitude for two hours. Echocardiograph measurements were performed every 20 minutes post-dive. Bubbles were counted and graded using the Germonpré and Eftedal and Brubakk method, respectively. No diver presented with symptoms of DCS following the dive or two hours post-dive at altitude. Despite inter- and intra-diver variability of VGE grade following the dives, the majority (11/20 dives) presented a peak VGE Grade 0, three VGE Grade 1, one VGE Grade 2, four VGE Grade 3, and one VGE Grade 4. Using the Cross correction method for a 66-fsw dive at 12,000 feet of altitude resulted in a relatively low decompression stress and no cases of DCS.

Acclimatization to diving: a systematic review.

Multiday hyperbaric exposure has been shown to reduce the incidence of decompression sickness (DCS) of compressed-air workers. This effect, termed acclimatization, has been addressed in a number of studies, but no comprehensive review has been published. This systematic review reports the findings of a literature search. PubMed, Ovid Embase, The Cochrane Library and Rubicon Research Repository were searched for studies reporting DCS incidence, venous gas embolism (VGE) or subjective health reports after multiday hyperbaric exposure in man and experimental animals. Twenty-nine studies fulfilled inclusion criteria. Three epidemiological studies reported statistically significant acclimatization to DCS in compressed-air workers after multiday hyperbaric exposure. One experimental study observed less itching after standardized simulated dives. Two human experimental studies reported lower DCS incidence after multiday immersed diving. Acclimatization to DCS has been observed in six animal species. Multiday diving had less consistent effect on VGE after hyperbaric exposure in man. Four studies observed acclimatization while no statistically significant acclimatization was reported in the remaining eight studies. A questionnaire study did not report any change in self-perceived health after multiday diving. This systematic review has not identified any study suggesting a sensitizing effect of multiday diving, and there is a lack of data supporting benefit of a day off diving after a certain number of consecutive diving days. The results suggest that multiday hyperbaric exposure probably will have an acclimatizing effect and protects from DCS. The mechanisms causing acclimatization, extent of protection and optimal procedure for acclimatization has been insufficiently investigated.

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.

Health care worker decompression sickness: incidence, risk and mitigation.

Inadvertent exposure to radiation, chemical agents and biological factors are well recognized hazards associated with the health care delivery system. Less well appreciated yet no less harmful is risk of decompression sickness in those who accompany patients as inside attendants (IAs) during provision of hyperbaric oxygen therapy. Unlike the above hazards where avoidance is practiced, IA exposure to decompression sickness risk is unavoidable. While overall incidence is low, when calculated as number of cases over number of exposures or potential for a case during any given exposure, employee cumulative risk, defined here as number of cases over number of IAs, or risk that an IA may suffer a case, is not. Commonly, this unique occupational environmental injury responds favorably to therapeutic recompression and a period of recuperation. There are, however, permanent and career-ending consequences, and at least two nurses have succumbed to their decompression insults. The intent of this paper is to heighten awareness of hyperbaric attendant decompression sickness. It will serve as a review of reported cases and reconcile incidence against largely ignored individual worker risk. Mitigation strategies are summarized and an approach to more precisely identify risk factors that might prompt development of consensus screening standards is proposed.

Performance of the BBraun perfusor space syringe driver under hyperbaric conditions.

BACKGROUND: The BBraun Perfusor Space™ syringe driver is already in use by ambulance services and retrieval teams but has not previously been assessed for hyperbaric chamber use. METHODS: Pump flow accuracy was tested at rates between 1 and 40 ml· h⁻¹ using three different brands of 50 ml syringe. Function of the occlusion alarms was assessed using the same syringes. The hyperbaric profile involved pressurisation to 284 kPa at 30 kPa· min⁻¹, 30 min at 284 kPa and decompression at 30 kPa· min⁻¹. Output was recorded from differences in weight of collection containers. A single device was tested. RESULTS: Performance was highly dependent on the syringe type used, with two of the three 50 ml syringes used demonstrating 'stiction' at both low and high occlusion pressure alarm settings, most marked during pressurisation. On decompression from 284 kPa all syringes alarmed at significantly lower pressures. Because of the stiction problems only the flow measurements for the BBrown Omni¬ x 50 ml syringes are reported. At a pressure of 284 kPa, the difference between programmed and delivered rates was within the manufacturer's specification of 10%: at 40 ml· h⁻¹ (median variation 1.25%, IQR 0.5-1.7%), 10 ml· h⁻¹ (8.6%, IQR 8-9.2%), 5 ml· h⁻¹ (-8.8%, IQR - 1.6-8.8%) and 1 ml· h⁻¹ (-4%, IQR 4-12%). Pressurisation was associated with significantly lower flow rates whilst decompression was associated with significantly increased rates. Limited testing at 405 kPa was also within the manufacturer's specifications. CONCLUSION: A BBraun Infusor Space syringe driver performed within acceptable performance criteria but is highly dependent on syringe type and flow rates. The potential for the device to under deliver on pressurisation and over deliver on depressurisation, however, suggests vigilance and appropriate rate adjustments may be necessary during these phases.

Preconditioning to Reduce Decompression Stress in Scuba Divers.

BACKGROUND: Using ultrasound imaging, vascular gas emboli (VGE) are observed after asymptomatic scuba dives and are considered a key element in the potential development of decompression sickness (DCS). Diving is also accompanied with vascular dysfunction, as measured by flow-mediated dilation (FMD). Previous studies showed significant intersubject variability to VGE for the same diving exposure and demonstrated that VGE can be reduced with even a single pre-dive intervention. Several preconditioning methods have been reported recently, seemingly acting either on VGE quantity or on endothelial inflammatory markers. METHODS: Nine male divers who consistently showed VGE postdive performed a standardized deep pool dive (33 m/108 ft, 20 min in 33°C water temperature) to investigate the effect of three different preconditioning interventions: heat exposure (a 30-min session of dry infrared sauna), whole-body vibration (a 30-min session on a vibration mattress), and dark chocolate ingestion (30 g of chocolate containing 86% cocoa). Dives were made one day per week and interventions were administered in a randomized order. RESULTS: These interventions were shown to selectively reduce VGE, FMD, or both compared to control dives. Vibration had an effect on VGE (39.54%, SEM 16.3%) but not on FMD postdive. Sauna had effects on both parameters (VGE: 26.64%, SEM 10.4%; FMD: 102.7%, SEM 2.1%), whereas chocolate only improved FMD (102.5%, SEM 1.7%). DISCUSSION: This experiment, which had the same subjects perform all control and preconditioning dives in wet but completely standardized diving conditions, demonstrates that endothelial dysfunction appears to not be solely related to VGE.Germonpré P, Balestra C. Preconditioning to reduce decompression stress in scuba divers. Aerosp Med Hum Perform. 2017; 88(2):114-120.

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.

Hyperbaric oxygen pretreatment and preconditioning.

Exposure to hyperbaric oxygen (HBO2) before a crucial event, with the plan to create a preventing therapeutic situation, has been defined "preconditioning" and is emerging as a useful adjunct both in diving medicine as well before ischemic or inflammatory events. Oxygen pre-breathing before diving has been extensively documented in recreational, technical, commercial and military diving for tissue denitrogenation, resulting in reduced post-diving bubble loads, reduced decompression requirements and more rapid return to normal platelet function after a decompression. Preoxygenation at high atmospheric pressure has also been used in patients before exposure to clinical situations with beneficial effects, but the mechanisms of action have not yet been ascertained. During the reperfusion of ischemic tissue, oxygenated blood increases numbers and activities of oxidants generated in tissues. Previous reports showed that HBO2 preconditioning caused the activation of antioxidative enzymes and related genes in the central nervous system, including catalase (CAT), superoxide dismutase and heme oxygenase-1. Despite the increasing number of basic science publications on this issue, studies describing HBO2 preconditioning in the clinical practice remain scarce. To date, only a few studies have investigated the preconditioning effects of HBO2 in relation to the human brain and myocardium with robust and promising results.

Decompression tables for inside chamber attendants working at altitude.

INTRODUCTION: Hyperbaric oxygen (HBO2) multiplace chamber inside attendants (IAs) are at risk for decompression sickness (DCS). Standard decompression tables are formulated for sea-level use, not for use at altitude. METHODS: At Presbyterian/St. Luke's Medical Center (Denver, Colorado, 5,924 feet above sea level) and Intermountain Medical Center (Murray, Utah, 4,500 feet), the decompression obligation for IAs is managed with U.S. Navy Standard Air Tables corrected for altitude, Bühlmann Tables, and the Nobendem© calculator. IAs also breathe supplemental oxygen while compressed. Presbyterian/St. Luke's (0.83 atmospheres absolute/atm abs) uses gauge pressure, uncorrected for altitude, at 45 feet of sea water (fsw) (2.2 atm abs) for routine wound care HBO2 and 66 fsw (2.8 atm abs) for carbon monoxide/cyanide poisoning. Presbyterian/St. Luke's provides oxygen breathing for the IAs at 2.2 atm abs. At Intermountain (0.86 atm abs), HBO2 is provided at 2.0 atm abs for routine treatments and 3.0 atm abs for carbon monoxide poisoning. Intermountain IAs breathe intermittent 50% nitrogen/50% oxygen at 3.0 atm abs and 100% oxygen at 2.0 atm abs. The chamber profiles include a safety stop. RESULTS: From 1990-2013, Presbyterian/St. Luke's had 26,900 total IA exposures: 25,991 at 45 fsw (2.2 atm abs) and 646 at 66 fsw (2.8 atm abs); there have been four cases of IA DCS. From 2008-2013, Intermountain had 1,847 IA exposures: 1,832 at 2 atm abs and 15 at 3 atm abs, with one case of IA DCS. At both facilities, DCS incidents occurred soon after the chambers were placed into service. CONCLUSIONS: Based on these results, chamber inside attendant risk for DCS at increased altitude is low when the inside attendants breathe supplemental oxygen.

Chamber personnel's use of Nitrox 50 during hyperbaric oxygen treatment: a quality study--research report.

OBJECTIVE: We aimed to evaluate the feasibility and safety of using Nitrox 50 as breathing gas during attendance in a multiplace hyperbaric chamber. METHODS: Paper logs between Jan.-Dec. 2011 were reviewed to analyze nitrogen gas-loading, actual bottom time, total bottom time and surface interval time. With the use of the Norwegian Diving Tables nitrogen gas-loading was converted to Repetitive Group Letters. Symptoms of decompression sickness and health problems related to hyperbaric exposures were registered at weekly staff meetings. The chamber personnel breathed chamber air or Nitrox 50. RESULTS: 1,207 hyperbaric exposures were distributed to five chamber attendants and technicians, 14 doctors, and six nurses. Nitrox 50 was inhaled on 978 occasions (81.0%). Median nitrogen gas-loading after first pressurization complied with Repetitive Group Letter A (range A-E), second to C (range A-F), third to D (range A-F), fourth to E (range C-H), fifth to F (range C-H), and sixth to E (range B-G). No symptoms of decompression sickness were reported (95% CI 0.00-0.33%). CONCLUSION: Breathing Nitrox 50 during repetitive hyperbaric sessions seems to be feasible and safe while meeting high demands in number of treatment sessions and patient flow and with fewer people employed in the hyperbaric unit.

Vigabatrin prevents seizure in swine subjected to hyperbaric hyperoxia.

Oxygen is the most widely used therapeutic strategy to prevent and treat decompression sickness (DCS). Oxygen prebreathe (OPB) eliminated DCS in 20-kg swine after rapid decompression from saturation at 60 feet of seawater (fsw). However, hyperbaric oxygen (HBO) has risks. As oxygen partial pressure increases, so do its toxic effects. Central nervous system (CNS) oxygen toxicity is the most severe side effect, manifesting as seizure. An adjunctive therapeutic is needed to extend OPB strategies to deeper depths and prevent/delay seizure onset. The Food and Drug Administration-approved anti-epileptic vigabatrin has prevented HBO-induced seizures in rats up to 132 fsw. This study aimed to confirm the rat findings in a higher animal model and determine whether acute high-dose vigabatrin evokes retinotoxicity symptoms seen with chronic use clinically in humans. Vigabatrin dose escalation studies were conducted 20-kg swine exposed to HBO at 132 or 165 fsw. The saline group had seizure latencies of 7 and 11 min at 165 and 132 fsw, respectively. Vigabatrin at 180 mg/kg significantly increased latency (13 and 27 min at 165 and 132 fsw, respectively); 250 mg/kg abolished seizure activity at all depths. Functional electroretinogram and histology of the retinas showed no signs of retinal toxicity in any of the vigabatrin=treated animals. In the 250 mg/kg group there was no evidence of CNS oxygen toxicity; however, pulmonary oxygen toxicity limited HBO exposure. Together, the findings from this study show that vigabatrin therapy is efficacious at preventing CNS oxygen toxicity in swine, and a single dose is not acutely associated with retinotoxicity.

Effect of pre-breathing oxygen at different depth on oxidative status and calcium concentration in lymphocytes of scuba divers.

AIM: In-water pre-breathing oxygen at various depths reduces decompression-induced bubble formation and platelet activation, but it could induce side effects such as oxidative stress. The aim of this study was to investigate the effect of in-water pre-breathing oxygen, at different depths, on the oxidative status and intracellular calcium ([Ca(2+) ]i) of peripheral blood lymphocytes isolated from six divers. They participated in a 4-diving protocol. Two week recovery time was allowed between successive dives. Before diving, all divers, for 20 min, breathed normally at sea level (dive 1), 100% oxygen at sea level (dive 2), 100% oxygen at 6 msw (dive 3), 100% oxygen at 12 msw (dive 4). Then they dived to 30 msw for 20 min with air tank. METHODS: Blood samples were collected before and after each dive. Hydrogen peroxide (H(2) O(2) ) levels, catalase (CAT) activity, mRNA expression of CAT, glutathione peroxidase (GPx) and superoxide dismutase (SOD), and the [Ca(2+) ]i in lymphocytes were measured. RESULTS: The dives slightly decreased lymphocyte number and significantly reduced lymphocyte H(2) O(2) levels. CAT activity was higher after scuba diving and, dive 3 enhanced mRNA gene expression of CAT, GPx and SOD. The [Ca(2+) ]i was higher after dive 1 and 2 than pre-diving, while was maintained at pre-diving value after dive 3 and 4. CONCLUSION: Our results suggest that pre-breathing oxygen, in particular at 12 msw, may enhance lymphocyte antioxidant activity and reduce reactive oxygen species levels. Pre-breathing oxygen in water may also preserve calcium homeostasis, suggesting a protective role in the physiological lymphocyte cell functions.

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.

Preconditioning methods and mechanisms for preventing the risk of decompression sickness in scuba divers: a review.

Scuba divers are at risk of decompression sickness due to the excessive formation of gas bubbles in blood and tissues following ascent, with potentially subsequent neurological injuries. Since nonprovocative dive profiles are no guarantor of protection against this disease, novel means are required for its prevention including predive procedures that could induce more resistance to decompression stress. In this article, we review the recent studies describing the promising preconditioning methods that might operate on the attenuation of bubble formation believed to reduce the occurrence of decompression sickness. The main practical applications are simple and feasible predive measures such as endurance exercise in a warm environment, oral hydration, and normobaric oxygen breathing. Rheological changes affecting tissue perfusion, endothelial adaptation with nitric oxide pathway, up-regulation of cytoprotective proteins, and reduction of preexisting gas nuclei from which bubbles grow could be involved in this protective effect.

Hyperbaric oxygen preconditioning reduces the incidence of decompression sickness in rats via nitric oxide.

Divers are at risk of decompression sickness (DCS) when the ambient pressure decrease exceeds a critical threshold. Hyperbaric oxygen (HBO2) preconditioning has been used to prevent various injuries, but the protective effect on DCS has not been well explored. To investigate the prophylactic effect of HBO2 on DCS, rats were pretreated with HBO2 (250 kPa-60 minutes) (all the pressures described here are absolute pressure) for 18 hours before a simulated air dive (700 kPa-100 minutes) with fast decompression to the surface at the rate of 200 kPa/min (n=33). During the following 30 minutes, the rats walked in a 3 m/minute rotating cage and were monitored for signs of DCS. The control rats were pretreated with normobaric air (n=30), normoxic hyperbaric nitrox (250 kPa, 8.4% O2) (n=13), or N(G)-nitro-L-arginine methyl ester (L-NAME) 30 minutes before HBO2 exposure (n=13). Nitric oxide (NO) levels were recorded immediately and 18 hours after HBO2 exposure in the brain and spinal cord. The incidence of DCS in rats pretreated with HBO2 was 30.3%, which was significantly lower than those treated with normobaric air (63.3%) (p<0.05) or hyperbaric nitrox (61.5%) (p<0.05). The onset time of DCS of the rats pretreated with HBO2 was significantly delayed compared with those treated with air (p<0.05). L-NAME nullified the HBO2 preconditioning effect. HBO2 increased NO level in the rat brain and spinal cord right after exposure; this effect was inhibited by L-NAME. Taken together, HBO2 preconditioning reduced the incidence of DCS in rats, and NO was involved in the prophylactic effect.

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 from saturation using oxygen: its effect on DCS and RNA in large swine.

INTRODUCTION: The use of hyperbaric oxygen (HBO) to expedite decompression from saturation has not been proven and may increase risk of toxicity to the pulmonary system. To evaluate any benefit of HBO during decompression, we used a 70-kg swine model of saturation and examined lung tissue by microarray analysis for evidence of RNA regulation. METHODS: Unrestrained, non-sedated swine were compressed to 132 fsw (5 ATA) for 22 h to achieve saturation. Animals then underwent decompression on air (AirD) or HBO (HBOD) starting at 45 fsw (2.36 ATA). Animals were evaluated for Type I and Type II decompression sickness (DCS) for 24 h. Control (SHAM) animals were placed in the chamber for the same duration, but were not compressed. Animals were sacrificed 24 h after exposure and total RNA was isolated from lung samples for microarray hybridizations on the Affymetrix platform. RESULTS: There was no evidence of Type I DCS or severe cardiopulmonary DCS in any of the animals; abnormal gaits were noted only in the HBOD group (4/9).Three genes (nidogen 2, calcitonin-like receptor, and pentaxin-related gene) were significantly up-regulated in both the AirD and HBOD groups compared to controls. Three other genes (TN3, platelet basic protein, and cytochrome P450) were significantly down-regulated in both groups. CONCLUSIONS: HBO during decompression from saturation did not reduce the incidence of DCS. Gene regulation was apparent and similar in both the AirD and HBOD groups, particularly in genes related to immune function and cell signaling.

Acclimation to decompression sickness in rats.

Protection against decompression sickness (DCS) by acclimation to hyperbaric decompression has been hypothesized but never proven. We exposed rats to acclimation dives followed by a stressful "test" dive to determine whether acclimation occurred. Experiments were divided into two phases. Phase 1 rats were exposed to daily acclimation dives of hyperbaric air for 30 min followed by rapid decompression on one of the following regimens: 70 ft of seawater (fsw) for 9 days (L70), 70 fsw for 4 days (S70), 40 fsw for 9 days (L40), 40 fsw for 4 days (S40), or unpressurized sham exposure for 9 days (Control). On the day following the last exposure, all were subjected to a "test" dive (175 fsw, 60 min, rapid decompression). Both L70 and S70 rats had significantly lower incidences of DCS than Control rats (36% and 41% vs. 62%, respectively). DCS incidences for the other regimens were lower than in Control rats but without statistical significance. Phase 2 used the most protective regimen from phase 1 (L70); rats were exposed to L70 or a similar regimen with a less stressful staged decompression. Another group was exposed to a single acclimation dive (70 fsw/30 min) on the day before the test dive. We observed a nonsignificant trend for the rapidly decompressed L70 dives to be more protective than staged decompression dives (44% vs. 51% DCS incidence). The single acclimation dive regimen did not provide protection. We conclude that protection against DCS can be attained with acclimating exposures that do not themselves cause DCS. The deeper acclimation dive regimens (70 fsw) provided the most protection.