Inner ear decompression sickness following a shallow scuba dive

Inner Ear Decompression Sickness (IEDCS)--manifested by tinnitus, vertigo, nausea, vomiting, and hearing loss--is usually associated with deep air or mixed gas dives, and accompanied by other CNS symptoms of decompression sickness (DCS). Early recompression treatment is required in order to avoid permanent inner ear damage. We present an unusual case of a scuba diver suffering from IEDCS as the only manifestation of DCS following a short shallow scuba dive, successfully treated by U.S. Navy treatment table 6 and tranquilizers. This case suggests that diving medical personnel should be more aware of the possible occurrence of IEDCS among the wide population of sport scuba divers.     

Venous gas embolism after an open-water air dive and identical repetitive dive

Decompression tables indicate that a repetitive dive to the same depth as a first dive should be shortened to obtain the same probability of occurrence of decompression sickness (pDCS). Repetition protocols are based on small numbers, a reason for re-examination. Since venous gas embolism (VGE) and pDCS are related, one would expect a higher bubble grade (BG) of VGE after the repetitive dive without reducing bottom time. BGs were determined in 28 divers after a first and an identical repetitive air dive of 40 minutes to 20 meters of sea water. Doppler BG scores were transformed to log number of bubbles/cm2 (logB) to allow numerical analysis. With a previously published model (Model2), pDCS was calculated for the first dive and for both dives together. From pDCS, theoretical logBs were estimated with a pDCS-to-logB model constructed from literature data. However, pDCS the second dive was provided using conditional probability. This was achieved in Model2 and indirectly via tissue saturations. The combination of both models shows a significant increase of logB after the second dive, whereas the measurements showed an unexpected lower logB. These differences between measurements and model expectations are significant (p-values < 0.01). A reason for this discrepancy is uncertain. The most likely speculation would be that the divers, who were relatively old, did not perform physical activity for some days before the first dive. Our data suggest that, wisely, the first dive after a period of no exercise should be performed conservatively, particularly for older divers.     

Blood platelet count and severity of decompression sickness in rats after a provocative dive

INTRODUCTION: Previous animal studies reported that platelet count (PC) is decreased following decompression. Adherence and aggregation of platelets to the bubble surface has been demonstrated in severe decompression sickness (DCS). The present study was designed to clarify the relationship between post-dive platelet levels and the severity of DCS in a rat model. METHODS: A total of 57 male Sprague-Dawley rats were assigned to either one experimental group with a hyperbaric exposure (N = 22) or one control group (N = 27). Rats were compressed to 1000 kPa (90 msw) for 45 min while breathing air and decompressed to surface in 38 min with stops at 200, 160, and 130 kPa. Onset of neurological DCS and death time were recorded during a 120-min observation period after surfacing. In the control group, rats were maintained at atmospheric pressure in the same chamber for an equivalent period of time. Blood samples for PC were taken 30 min before and immediately after exposure in two groups. RESULTS: Blood PC after hyperbaric exposure had significantly decreased, whereas PC had increased in the control group. We found a correlation between % fall in PC and latency to death time. The platelet loss tended to decrease when fatal DCS was delayed. Rats suffering from severe DCS with a short latency to death presented a pronounced decline in platelets. DISCUSSION: The present study highlighted a relationship between the post-dive decrease in PC and DCS severity in rats. Platelet consumption could offer a new index for evaluating decompression stress.     

Risk factors for venous gas emboli after decompression from prolonged hyperbaric exposures

INTRODUCTION: The physical forces governing gas phase nucleation and growth in a liquid would predict less variation in the development of decompression sickness (DCS) than is known to occur in people. METHODS: In order to gain insight into the causes of biological susceptibility to DCS, we analyzed a dataset containing 250 human steady-state hyperbaric exposures using multivariate ordinal and linear regression analysis for relationships between venous gas emboli (VGE) and exposure parameters and subject characteristics. RESULTS: In both previously published data and new chamber exposure data, we found that the strongest predictor of VGE magnitude after decompression was the duration and depth of the hyperbaric exposure, as predicted. Of the subject factors, only age was significantly associated with VGE; body mass index (BMI) and gender were not. The relationship between age and VGE strengthened with decompression magnitude. DISCUSSION: These results suggest that the physiology of aging interacts with the mechanism of VGE generation, altering the risk of DCS after decompression.     

Central nervous system decompression sickness and venous gas emboli in hypobaric conditions

INTRODUCTION: Altitude decompression sickness (DCS) that involves the central nervous system (CNS) is a rare but potentially serious condition. Identification of early symptoms and signs of this condition might improve treatment. METHODS: We studied data from 26 protocols carried out in our laboratory over the period 1983-2003; all were designed to provoke DCS in a substantial proportion of subjects. The data set included 2843 cases. We classified subject-exposures that resulted in DCS as: 1) neurological DCS of peripheral and/or central origin (NEURO); 2) a subset of those that involved only the CNS (CNS); and 3) all other cases, i.e., DCS cases that did not have a neurological component (OTHER). For each case, echo imaging data were used to document whether venous gas emboli (VGE) were present, and their level was classified as: 1) any level, i.e., Grade 1 or higher (VGE-1); and 2) high level, Grade 4 (VGE-4). RESULTS: There were 1108 cases of altitude DCS in the database; 218 were classified as NEURO and 49 of those as CNS. VGE-1 were recorded in 83.8% of OTHER compared with 58.7% of NEURO and 55.1% of CNS (both p < 0.001 compared with OTHER). The corresponding values for VGE-4 were 48.8%, 37.0%, and 34.7% (p < 0.001, compared to OTHER). Hyperbaric oxygen (HBO) was used to treat about half of the CNS cases, while all other cases were treated with 2 h breathing 100% oxygen at ground level. DISCUSSION: Since only about half of the rare cases of hypobaric CNS DCS cases were accompanied by any level of VGE, echo imaging for bubbles may have limited application for use as a predictor of such cases.     

Exercise effects during diving and decompression on postdive venous gas emboli

BACKGROUND: Exercise and diving have generally been associated with an increased risk of decompression sickness (DCS), thus accounting for the lack of studies involving exercise during decompression. However, theoretical and observational evidence contrary to this association motivated the present investigation on the effects of moderate, intermittent exercise during diving and/or during decompression on venous gas emboli (VGE) activity following a dive. HYPOTHESIS: VGE observed at both the precordium and subclavian vein sites after diving should be reduced if moderate exercise is performed during decompression vs. remaining inactive. METHODS: In a water-filled hyperbaric chamber, 39 healthy male subjects were compressed to a pressure of 450 kPa (45 msw) for 30 min followed by 55 min of staged decompression. Subjects were either active or inactive at the bottom phase (450 kPa) and/or during the decompression. Activity comprised three 5-min intervals of moderate arm or leg exercise at the bottom and five such intervals during decompression. After decompression, VGE were monitored at the precordium and subclavian vein sites using Doppler detection. Bubble activity scores were converted to various indices and analyzed using non-parametric statistics. RESULTS: VGE activity was invariant as to whether subjects were active or sedentary during the bottom phase of the dive. However, it was significantly lower for all indices examined (p < 0.05) after dives in which exercise was performed during decompression vs. inactive decompression. CONCLUSION: Moderate, intermittent physical activity during decompression decreases VGE activity after diving.     

Age affects severity of venous gas emboli on decompression from 14.7 to 4.3 psia

INTRODUCTION: Variables that define who we are, such as age, weight and fitness level influence the risk of decompression sickness (DCS) and venous gas emboli (VGE) from diving and aviation decompressions. We focus on age since astronauts that perform space walks are approximately 10 yr older than our test subjects. Our null hypothesis is that age is not statistically associated with the VGE outcomes from decompression to 4.3 psia. METHODS: Our data are from 7 different NASA tests where 188 men and 50 women performed light exercise at 4.3 psia for planned exposures no less than 4 h. Prebreathe (PB) time on 100% oxygen ranged from 150-270 min, including ascent time, with exercise of different intensity and length being performed during the PB in four of the seven tests with 150 min of PB. Subjects were monitored for VGE in the pulmonary artery using a Doppler ultrasound bubble detector for a 4-min period every 12 min. There were six design variables; the presence or absence of lower body adynamia and five PB variables; plus five concomitant variables on physical characteristics: age, weight height, body mass index, and gender that were available for logistic regression (LR). We used LR models for the probability of DCS and VGE, and multinomial logit (ML) models for the probability of Spencer VGE Grades 0-IV at exposure times of 61, 95, 131, 183 min, and for the entire exposure. RESULTS: Age was significantly associated with VGE in both the LR and ML models, so we reject the null hypothesis. Lower body adynamia was significant for all responses. CONCLUSIONS: Our selection of tests produced a wide range of the explanatory variables, but only age, lower body adynamia, height, and total PB time was helpful in various combinations to model the probability of DCS and VGE.     

Pulmonary decompression sickness at altitude: early symptoms and circulating gas emboli

INTRODUCTION: Pulmonary altitude decompression sickness (DCS) is a rare condition. 'Chokes' which are characterized by the triad of substernal pain, cough, and dyspnea, are considered to be associated with severe accumulation of gas bubbles in the pulmonary capillaries and may rapidly develop into a life-threatening medical emergency. This study was aimed at characterizing early symptomatology and the appearance of venous gas emboli (VGE). METHODS: Symptoms of simulated-altitude DCS and VGE (with echo-imaging ultrasound) were analyzed in 468 subjects who participated in 22 high altitude hypobaric chamber research protocols from 1983 to 2001 at Brooks Air Force Base, TX. RESULTS: Of 2525 subject-exposures to simulated altitude, 1030 (41%) had symptoms of DCS. Only 29 of those included DCS-related pulmonary symptoms. Of these, only 3 subjects had all three pulmonary symptoms of chokes; 9 subjects had two of the pulmonary symptoms; and 17 subjects had only one. Of the 29 subject-exposures with pulmonary symptoms, 27 had VGE and 21 had severe VGE. The mean onset times of VGE and symptoms in the 29 subject-exposures were 42 +/- 30 min and 109 +/- 61 min, respectively. In 15 subjects, the symptoms disappeared during recompression to ground level followed by 2 h of oxygen breathing. In the remaining 14 cases, the symptoms disappeared with immediate hyperbaric oxygen treatment. CONCLUSIONS: Pulmonary altitude DCS or chokes is confirmed to be a rare condition. Our data showed that when diagnosed early, recompression to ground level pressure and/or hyperbaric oxygen treatment was 100% successful in resolving the symptoms.     

潜艇脱险中极快速减压后大鼠小胶质细胞与神经元凋亡的变化

目的 研究成年大鼠极快速减压致中枢神经损伤后脑组织内小胶质细胞的变化及其与损伤后神经元凋亡的关系。方法 采用1MPa暴露5．5min、50s快速减压制备SD大鼠中枢减压损伤模型,在减压后6、24、48、72h取材,分别用FITC标记的凝集素B4（IB4）标记小胶质细胞和原位末端TUNEL。法标记凋亡神经元细胞。结果 快速减压后6h组可见少量IB4阳性小胶质细胞;24h组达高峰（P〈0．01）;48h组阳性小胶质细胞数量有所下降,但仍高于6h组（P〈0．01）;72h组阳性小胶质细胞数量明显下降。6h组仅见少量散在TUNEL,阳性细胞;48h组达高峰（P〈0．01）;72组阳性细胞数量有所下降,但仍高于6h组（P〈0．01）。凝集素阳性小胶质细胞分布区域与神经元凋亡分布区域一致,达到高峰的时间前者先于后者,两者的变化趋势相同（r=O．645,P〈0．01）。结论 不安全极快速减压致中枢型减压病的中枢神经损伤中存在神经元凋亡和小胶质细胞的活化,激活的小胶质细胞可能参与了快速减压后的神经元凋亡过程。     

Glutathione in blood cells decreases without DNA breaks after a simulated saturation dive to 250 msw

INTRODUCTION: Saturation diving involves exposure to high pressure and elevated oxygen level. The impact of cellular defense systems like glutathione in protecting cells against oxidative DNA damage seems unclear. The aim of the present study was, therefore, to investigate whether diving conditions would affect blood cell glutathione and thus alter the mononuclear cells' (MNC) susceptibility to oxidative DNA damage. METHODS: Eight subjects participated in a simulated saturation dive to 2.6 MPa (250 msw) lasting 19.3 d (0.8 d compression, 6.6 d bottom phase, 11.9 d decompression) breathing helium-oxygen with PO2 ranging from 35 to 70 kPa (3.5-7.0 msw). Blood samples collected before compression and after decompression were analyzed for glutathione content and single-stranded DNA breaks. RESULTS: The results demonstrate for the first time that a simulated saturation dive decreased glutathione content in peripheral blood cells (32% decrease in MNC), and that the decrease was most pronounced in the erythrocytes (45%). Remarkably, no single-stranded DNA breaks could be detected in the MNC despite the low glutathione level. DISCUSSION: The results suggest that glutathione is a useful indicator of oxidative stress and that a low glutathione level represents no significant harm to the blood cells in the absence of other toxic agents. The lack of DNA strand breaks suggests that protection against oxidative DNA damage was mainly provided by mechanisms other than the glutathione system. Although previous investigations point to hyperoxia as the most plausible explanation for the present observations, the effect of high pressure cannot be excluded.     

Diffusing capacity and spirometry following a 60-minute dive to 4.5 meters.

The purpose of this study was to assess the contribution of SCUBA to the pulmonary effects of diving to 4.5 meters depth in healthy subjects using a randomized crossover control condition. Ten healthy divers performed two 60-minute 'dives' using SCUBA in a swimming pool. The non-immersed 1 ATA SCUBA control exposure took place at ambient pressure in the laboratory. Thirty minutes prior to, and 30 and 90 minutes post-exposure, FVC (forced vital capacity), FEV1.0 (forced expired volume), peak expiratory flow rate (PEFR), diffusing capacity (DL(co)), heart rate (HR) and temperature were measured. No significant differences were noted in HR, temperature or spirometry between the two conditions. A significant reduction in diffusing capacity occurred at 30 and 90 minutes after the pool dive (9.3% and 15.1%, respectively, p < 0.05). There was no concordant change in DL(co) following the non-immersed 1 ATA SCUBA control. Thus, a pool dive to 4.5 meters for 60 minutes causes a decrease in DL(co), without a change in spirometry, while breathing from SCUBA equipment without immersion causes no significant change in lung function.     

Isoproterenol accelerates decompression sickness and death after saturation dives in swine

BACKGROUND: Disabled submarine (DISSUB) survivors are expected to achieve inert gas tissue saturation that would likely cause severe decompression sickness (DCS). Rescue procedures in a DISSUB scenario cannot accommodate a staged decompression and the availability of recompression treatment chambers is limited. Alternatives to the standard recompression procedures for treating DCS are needed. Experimentally, isoproterenol has successfully addressed many underlying physiological concerns expected to result in cardiopulmonary DCS in this group. HYPOTHESIS: We hypothesized that isoproterenol would reduce the incidence of cardiopulmonary DCS in a saturation dropout model. METHODS: Yorkshire swine (21.8 +/- 1.68 kg) were fitted with an external jugular catheter and compressed to 4.33 ATA in a dry chamber for 22 h. They were infused with isoproterenol (0.002 mg x kg(-1)) while still at depth and returned to the surface without decompression stops. They received additional infusions every 10 min throughout a 2-h observation period. Signs of DCS were recorded to the nearest minute. RESULTS: Isoproterenol administration resulted in a significant increase in the incidence of severe cardiopulmonary DCS (13/34 control vs. 12/18 isoproterenol) and death from DCS (10/34 control vs. 11/18 isoproterenol). There was no difference in the incidence of severe neurological DCS. CONCLUSIONS: Administering isoproterenol as an intervention/treatment for DCS significantly increases the risk of cardiopulmonary DCS and death following saturation dropout in 20-kg swine. As an adjunctive therapy or alternative to staged decompression, isoproterenol in the dose regimen delivered here is not expected to improve outcome in a DISSUB mass casualty scenario.     

Cardiovascular and endocrine responses to 90 degree tilt during a 35-day saturation dive to 46 and 37 ATA

INTRODUCTION: Hyperbaria-induced diuresis is accompanied by decreased basal and stimulated release of arginine vasopressin (AVP) and decreased blood volume possibly contributing to the reported orthostatic intolerance. Since hyperosmolality is not a consistent finding, the explanation of blood volume reduction at hyperbaria must involve an osmotic component to the diuresis. Investigations of a possible involvement of atrial natriuretic peptide (ANP) to the hyperbaric diuresis have revealed mixed results. METHODS: Urinary excretion of electrolytes, AVP, and aidosterone were measured in four male subjects studied at 1 atmosphere absolute (ATA) and at 46 and 37 ATA (0.5 atmospheres pressure O2: 5% N2: remainder He) during a 35-d saturation dive. Also, the supine and 90 degrees tilt-stimulated plasma levels of AVP, plasma renin activity (PRA), and aldosterone, and the suppressed responses of ANP and the cardiovascular responses to tilt were determined at these pressures. RESULTS: Tilt-stimulated levels of PRA were increased two- to threefold and the AVP response was eliminated throughout hyperbaria, except in two episodes of tilt-induced syncope where AVP was elevated 10- to 20-fold. This pattern supports most previous reports. Contrary to some reports, both supine and tilt-suppressed levels of ANP were reduced by about 50% at all three tilt experiments conducted at hyperbaria compared to predive control values. DISCUSSION: These results suggest an altered ANP response at pressures of 37 ATA or greater, which is consistent with an appropriate ANP response to blood volume reduction and further suggest that the hyperbaric diuresis is not dependent on increased ANP.     

模拟氦氧饱和潜水实验中监测潜水员尿量及尿电解质的作用

目的 探讨模拟2.6 MPa氦氧饱和潜水暴露时潜水员尿量及尿电解质变化对潜水员健康干预的监护作用.方法 7名健康男性潜水员参加模拟250 m氦氧饱和潜水,在暴露前、中、后每日取晨尿和24h尿检测尿常规、尿量、尿电解质、肌酐及N-乙酰-β-D-氨基葡萄糖苷酶(NAG)排泄量.结果参试潜水员尿常规在高压暴露过程中没有明显变化;尿量在暴露于2.0 MPa以上压力时略有增高,但无统计学意义(P＞0.05):尿Na+、K+、Cl-、Ca2+、Mg2+、NAG酶在高压下排泄减少(P＜0.05),尤以钙减少明显且持续时间长,但在减压后1周基本恢复至正常水平.结论 模拟2.6 MPa氦氧饱和潜水暴露过程中潜水员尿量和尿电解质排泄存在波动,检测尿量和尿电解质排泄量可为舱内潜水员的健康干预提供参考依据.     

Regenerative capacity of normal and irradiated liver following partial hepatectomy in rats

Purpose:?To investigate the regenerative capacity and proliferation related to cell cycle modulators in irradiated livers after partial hepatectomy (PH) in rats.

Methods and materials:?Two experimental groups were given a single dose of either 4-Gy or 8-Gy photon radiation to the whole liver following PH. The control group underwent only PH, without irradiation. The liver specimens were analysed for apoptosis, proliferation and cell cycle related genes between 0.5 and 12 days.

Results:?Mean change in weight of the remnant liver in the 8-Gy group was significantly lower than in the control and 4-Gy groups. The apex of proliferating cell nuclear antigen labelling and bromodeoxyuridine incorporation index in two irradiated groups were also apparently lower than that in control group. After PH, transforming growth factor beta-1 (TGFβ1), and the type II receptor of TGFβ (TGFβR-II), anti-tumour protein 53(p53) and anti-tumour protein21(p21) protein expression in the irradiated livers was higher than in unirradiated ones. Significant apoptosis was noted in 8-Gy group. However, the maximal value of hepatocyte growth factor (HGF) mRNA and protein expression in the irradiated group was suppressed and restoration of liver function was delayed.

Conclusion:?Whole liver lower dose irradiation can attenuate regenerative capacity following partial hepatectomy in rats.     

Pharmacological intervention to the inflammatory response from decompression sickness in rats

INTRODUCTION: Venous bubbles resulting from experimental decompression sickness (DCS) may cause an inflammatory-like reaction with activation of granulocytes and release of metabolites from arachidonic acid. The release of cyclooxygenase and lipoxygenase pathway mediated metabolites, namely thromboxane B2 (TXB2) and leukotriene E4 (LTE4) likely contribute to this overall DCS response. In the present study we examined the effect on DCS outcome of several agents affecting both pathways. METHODS: Indomethacin and acetylsalicylic acid were administered to study the cyclooxygenase pathway mediators, Zafirlukast and Zileuton to study inhibition of the lipoxygenase pathway, and isoproterenol for its beta-agonist effects. The agents were administered to randomly selected Sprague-Dawley rats prior to compression to 683 kPa for 60 min. Following 60 min recovery post-decompression, DCS evaluation included: gross symptoms; pulmonary edema; bronchoalveolar lavage and pleural fluid protein; white blood cell and differential cell counts; and urine, bronchoalveolar lavage, and plasma TXB2 and LTE4 analysis. RESULTS: The results indicate that both Zafirlukast and Zileuton reduced the reported DCS symptoms, pulmonary edema, pleural and bronchoalveolar lavage protein levels, white blood cell counts in the pleural and bronchoalveolar lavage, and leukotriene levels in the bronchoalveolar lavage vs. that of vehicle-treated rats exposed to compression/decompression. The effect of these agents on pleural and bronchial alveolar protein levels demonstrated protective effects on microvascular permeability. Acetylsalicylic acid and indomethacin treatment had less effect on reducing inflammatory-induced changes. DISCUSSION: The effect of inflammatory-like responses to DCS can be altered with pharmacological intervention given prior to compression.     

Probability of altitude decompression sickness following a drop in pressure from 840 to 308 mm Hg

The decompression from the hyperbaric air atmosphere with the pressure 840+/-5 mm Hg and subsequent 40 min exposure to the hypobaric atmosphere 308+/-1 mm Hg containing 40 to 95% O2 cause a decompression disease in 5-40% cases. The probability of the disease depends on the duration of nitrogen saturation at an increased pressure, physical fitness and individual susceptibility to decompression sickness.     

Venous thromboembolism in passengers following a 12-h flight: a case-control study

OBJECTIVES: There has recently been great interest in the possible relationship between air travel and venous thromboembolism (VTE). Based on a case-control survey, we measured the frequency of VTE, associated risk factors (RFs), and factors influencing the onset of pulmonary embolism (PE) or deep vein thrombosis (DVT). METHODS: The study was conducted over 1 yr. A questionnaire was sent to physicians. Patients with a diagnosis of VTE were included, provided they had traveled from France to Reunion Island. RESULTS: Over 46 cases, 33 patients showed DVT and 13 PE. RFs for VTE were present in 38 patients (82%). On comparing RFs between study and control groups, we found no differences in age, gender, alcohol, sleep-inducing drug consumption, seat allocation, or estroprogestative treatment. RFs were significantly higher in the VTE group at p < 0.005: history of previous VTE (OR 63.3), recent trauma (OR 13.6), presence of varicose veins (OR 10), obesity (OR 9.6), immobility during flight (9.3), and cardiac disease (OR 8.9). For patients with DVT or PE, no differences were observed in comparing RFs. The PE group was older and mortality occurred only in this group. The number of displacements during flight (p < 0.009) and complete immobility (p < 0.001) were strongly related with onset of PE. Delay of symptoms was less than 24 h in 69% of PE cases compared with 21% of DVT cases (p < 0.004). CONCLUSION: Long-duration air travel VTE is associated with other underlying thromboembolic RFs. Low mobility during flight is a striking modifiable RF of developing PE. Travelers with RFs for VTE should be advised to increase their mobility.     

专家评分法及秩和比法在模拟大深度饱和潜水实验潜水员选拔中的应用

目的 选拔出参加模拟大深度氦氧饱和潜水实验符合要求的潜水员.方法 根据7名潜水员在模拟250 m潜水实验中的脑干听觉诱发电位、神经行为功能、脑电图、手指震颤、主观症状、体能和心率变异性7种生理、心理指标,采取专家评分法确定各种指标的权重,用秩和比法得到各潜水员的综合排名.结果 参加最终实验的4名潜水员在480 m饱和493 m巡潜时的表现与他们在模拟250 m潜水阶段综合排名的相关系数为1 (P＜0.01),潜水员在加压过程中出现高压神经综合征的先后次序亦验证了该排名.结论 在有较浅深度预演模拟潜水的情况下,利用潜水员在预演时的生理、心理参数,采取专家评分法及秩和比法可以有效预测他们在更大深度的作业能力.该综合评价方法不失为一种有效的潜水员选拔方案.     

Altitude decompression sickness between 6858 and 9144 m following a 1-h prebreathe

INTRODUCTION: The zero prebreathe altitude threshold for developing 5% decompression sickness (DCS) symptoms in men has been reported to be 6248 m (20,500 ft). However, such an altitude threshold when 1 h of oxygen prebreathe is used has not been well documented and was the primary purpose of this study. METHODS: The 51 male human subjects were exposed to 9144 m (30,000 ft), 8382 m (27,500 ft), 7620 m (25,000 ft), and/or 6858 m (22,500 ft) for 8 h. They were monitored for symptoms of DCS and venous gas emboli (VGE). RESULTS: DCS symptom incidence after 4 h of exposure decreased with exposure altitude from 87% at 9144 m to 26% at 6858 m. VGE were lower during the 4-h 6858-m exposures (32%) than at the higher altitudes (76-85%). The symptom incidences during the first 4 h of exposure were lower at 6858 m and 7620 m following a 1-h prebreathe as compared with analogous zero-prebreathe exposures. There were no differences between incidences of VGE or DCS at any of the four altitudes after 8 vs. 4 h of exposure. CONCLUSION: The altitude threshold for 5% DCS symptoms is below 6858 m after 1 h of prebreathe. However, during 6858-m and 7620-m exposures, a 1-h prebreathe is highly beneficial in reducing DCS incidence and delaying the onset of DCS, keeping the incidence to less than 6% during the first 90 min of exposure. Use of 4-h vs. 8-h exposures does not appear to underestimate DCS risk at or above 7620 m.