Delayed effect of nitric oxide synthase inhibition on the survival of rats after acute decompression.

AIM: The formation of bubbles in the blood stream together with the ensuing sickness after rapid decompression is assumed to depend on the physiological condition of the vascular system. In order to gain insight into the vascular function of nitric oxide in acute decompression sickness, the effects of the nitric oxide synthase inhibition by N(omega)-nitro-L-arginine methyl ester was studied in rats. METHODS: Wistar rats under anaesthesia were exposed to hyperbaric conditions for two hours and decompressed approximately 2.5 hours after a single subcutaneous injection of N(omega)-nitro-L-arginine methyl ester. Scalar doses and different pressures were tested. RESULTS: The fraction of the rats that died after decompression was greater in rats treated with N(omega)-nitro-L-arginine methyl ester at doses greater than 8 mg Kg-1 body weight compared to untreated rats. CONCLUSION: Although we have not excluded effects of nitric oxide synthase inhibition on distribution of perfusion and therefore inert gas elimination from tissue during decompression as a factor, this result highlights a delayed benefit of nitric oxide synthase activity in preventing death in acute decompression sickness.     

高压氧预暴露对急性氧中毒大鼠模型惊厥潜伏期影响的实验研究

目的 研究高压氧预暴露对大鼠急性氧中毒潜伏期的影响并探讨其机制.方法 将40只Sprague-Dawley(SD)大鼠随机分为对照组和高压氧预暴露组,每组20只,其中高压氧预暴露组于高压纯氧(0.3 MPa)下暴露20 min,然后减至常压行空气通风20 min,如此循环4次.24 h后,将2组大鼠暴露于高压纯氧(0.5 MPa),观察40 min.检测指标包括惊厥潜伏期变化、大鼠脑组织中超氧化物歧化酶(SOD)活性和一氧化氮(NO)含量变化,进行HE染色以观察脑组织病理改变.结果 高压氧预暴露后,大鼠惊厥潜伏期[(29.79±2.13)min]比对照组[(24.25±3.76)min]延长,脑组织NO含量[(2.93±0.39)nmol/g]比对照组[(7.46±1.11)nmol/g]减少,而SOD活性与HE染色结果 显示2组差异无统计学意义.结论 高压氧预暴露可以延长大鼠惊厥潜伏期,其机制可能是高压氧降低了脑组织中的NO含量.     

吸氧排氮对家兔低气压暴露时气泡产生的影响

目的 探讨不同时间的吸氧排氮方案对高空减压病的预防效果。方法 24只家兔随机分为对照组、吸氧排氮30、60和120min组4组。麻醉后行机械通气,分别吸氧排氮0、30、60和120min后上升至11000m停留30min,用超声多普勒技术检测气泡产生情况。结果 高空减压时气泡首次检出时间随着吸氧排氮时间的增加而延长,吸氧排氮60min和120min组家兔气泡首次检出时间较对照组显著延长(P＜0．01),气泡首次检出时间与吸氧排氮时间呈正相关关系(P＜0．01);累积气泡数随着吸氧排氮时间的增加而减少,吸氧排氮60min和120min组家兔累积气泡数较对照组显著减少(P＜0．01),累积气泡数与吸氧排氮时间呈负相关关系(P＜0．01)。结论 吸氧排氮60min和120min两种方案可以显著减少兔由地面上升到11000m高空减压时气泡的产生。     

快速减压后大鼠模型视网膜电生理的变化

目的 观察快速减压(RD)后大鼠视网膜电图(ERG)的变化,并探讨减压病造成视网膜早期功能损伤的特点。方法 20只大鼠按数字表法随机分为4组,分别为正常对照(NC)组、安全减压(SD)组、快速减压处理后0 h(RD0)组和6 h(RD6)组,SD组、快速减压处理各组大鼠暴露于加压舱内,舱内气压在30 s内升至1.0 MPa,维持5.5 min,快速减压各组打开放气阀用55 s减至常压,SD组采用动物安全减压方案减到常压。按照国际临床视觉电生理学会的标准化方案,采用国特医疗系统和银-氯化银角膜电极以及银针电极对大鼠进行暗视视网膜电图(Scot-ERG)、振荡电位(OPs)、明视视网膜电图(L-ERG)记录。结果 快速减压后大鼠ERGa、b波以及OPs O2波幅值降低,潜伏期明显延长。快速减压后6h,Scot-ERG b波和OPs O2波幅值增加,RD6组[b波(134.5±27.9) μV,O2波(27.1±9.2)μV]较RD0组[b波(56.5±21.1) μV,O2波(8.1±1.9) μV]高(P＜0.05)。SD组比RD0组和RD6组视网膜电活动受抑制程度轻,SD组Scot-ERG b波和OPs O2波幅值[b波(266.5±25.2) μV,02波(44.1±5.6) μV]高于快速减压后RD0组和RD6组(P＜0.05)。结论 快速减压会造成大鼠视网膜电生理异常,安全减压可有助于减轻这种功能损伤。     

Optic neuropathy following an altitude exposure

This case report describes a 20-yr-old man who presented with retro-orbital pain and blurred vision in his left eye 3 wk after an altitude exposure in a hypobaric chamber. He was found to have significant deficits in color vision and visual fields consistent with an optic neuropathy in his left eye. The patient was diagnosed with decompression sickness and treated with hyperbaric oxygen with a U.S. Navy Treatment Table VI. All signs and symptoms resolved with a single hyperbaric oxygen treatment but recurred. A head MRI revealed a left frontoethmoid sinus opacity. A concomitant sinusitis was diagnosed. The patient had full resolution of symptoms after a total of four hyperbaric oxygen treatments and antibiotic therapy at 6-wk follow-up. Although a para-infectious etiology for this patient's optic neuropathy cannot be excluded, his history of altitude exposure and significant, rapid response to hyperbaric oxygen treatment strongly implies decompression sickness in this case.     

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.     

辐射合并减压暴露致大鼠急性肺损伤的效应观察

目的 探讨不同剂量辐射暴露对快速上浮脱险致大鼠减压病急性肺损伤及死亡率的影响。 方法 53只SD大鼠按体重分层后以随机数表法分为5组:空白对照组（10只）、单纯减压组（10只）、4 Gy照射+减压组（11只）、6 Gy照射+减压组（11只）以及8 Gy照射+减压组（11只）。照射组大鼠先进行4、6、8 Gy不同剂量60Co γ射线全身照射,空白对照组及单纯减压组大鼠在相同环境下不进行照射;照射结束后1 h各减压组再进行减压处理实验（57 m停留45 min后,37 s快速减压至大气压）,观察各组大鼠死亡率、肺湿干重比、肺组织病理损伤程度以及肺泡灌洗液中炎症因子和氧化应激相关分子水平的变化。各组大鼠死亡率的比较采用卡方检验,其他指标的比较采用单因素方差分析,进一步两两比较采用LSD-t检验。 结果 与空白对照组比较,各实验组大鼠死亡数量和肺湿干重比均增加,6 Gy照射+减压组和8 Gy照射+减压组大鼠肺湿干重比显著增加,且差异有统计学意义（F=3.096,LSD-t=2.758、2.959;均P<0.05）;各实验组大鼠肺组织病理损伤明显,其中6 Gy照射+减压组和8 Gy照射+减压组更为显著;各实验组大鼠肺泡灌洗液中白细胞介素1β（IL-1β）、白细胞介素6（IL-6）、肿瘤坏死因子α（TNF-α）和丙二醛（MDA）水平显著增加,且差异有统计学意义（F=45.680~78.270,均P<0.01）,超氧化物歧化酶（SOD）活力和谷胱甘肽过氧化物酶（GSH-Px）水平显著下降,且差异有统计学意义（F=35.720、51.370,均P<0.01）。与单纯减压组比较,4 Gy照射+减压组和8 Gy照射+减压组大鼠死亡数量增加,但死亡率的差异无统计学意义（χ2=7.925,P>0.05）;各照射组大鼠肺湿干重比虽有上升趋势,但差异无统计学意义（LSD-t=0.901、1.818、2.020,均P>0.05）;各照射组大鼠肺组织病理损伤有不同程度的加重,其中8 Gy照射+减压组损伤程度最重;各照射组大鼠肺泡灌洗液中炎症因子（IL-1β、IL-6、TNF-α）和氧化应激相关分子（SOD、GSH-Px、MDA）均变化显著（LSD-t=3.081~8.265,均P<0.01）,其中6 Gy照射+减压组变化最为显著。 结论 辐射会加重快速上浮脱险造成的肺组织炎症和氧化应激损伤,表现为肺组织病理损伤程度加重及死亡率增加,从而增加快速上浮脱险致减压病发生的风险。     

Venous gas emboli in normal and dehydrated rats following decompression from a saturation dive

INTRODUCTION: Dehydration may increase the risk for decompression sickness (DCS). Since DCS most probably is caused by endogenous gas phase formation, we hypothesized that decompression will induce more venous gas emboli (VGE) in dehydrated rats compared to controls. METHODS: Two groups of rats were pressurized to 0.5 MPa (5 ATA) on heliox for 16 h, and thereafter decompressed to atmospheric pressure at a rate of 0.3 MPa x min(-1). The nine control rats had free access to water ad libitum whereas the eight dehydrated rats were water-deprived for 48 h before decompression. During and after decompression, VGE was measured in the vena cava for 60 min with the Doppler technique and graded into six bubble grade (BG) categories. Body mass (BM), and food and water intake were registered daily, and venous blood samples were taken before and after pressure exposure. RESULTS: Serum osmolality and hematocrit increased significantly in dehydrated rats (306 +/- 5.2 to 315 +/- 7.3 mosmol x kg(-1) and 39.3 +/- 4.9 to 49.6 +/- 5.2%) but not in controls (300 +/- 8.9 to 303 +/- 6.7 mosmol x kg(-1) and 40.3 +/- 5.2 to 41.4 +/- 6.1%). Plasma volume decreased by 9.2% (P < 0.05) and 2.8% (n.s.) in dehydrated and control rats. VGE were detected in all control animals (average BG: 2.8 +/- 1.9), but only in four water-deprived rats (BG: 1.6 +/- 2.2). This difference was not significant. CONCLUSIONS: Our experiments do not support the idea that dehydration increases circulatory VGE.     

Decompression schedule optimization with an isoprobabilistic risk of decompression sickness

INTRODUCTION: Divers use decompression schedules to reduce the probability of occurrence of decompression sickness when returning to the surface at the end of a dive. The probability of decompression sickness resulting from these schedules varies across different dives and the models used to generate them. Usually the diver is unaware of this variance in risk. This paper describes an investigation into the feasibility of producing optimized iso-probabilistic decompression schedules that minimize the time it takes for a diver to reach the surface. METHODS: The decompression schedules were optimized using the sequential quadratic programming method (SQP), which minimizes the ascent time for a given probability of decompression sickness. The U.S. linear-exponential multi-gas model was used to calculate an estimate of the probability of decompression sickness for a given dive. In particular 1.3-bar oxygen in helium rebreather bounce dives to between 18 m and 81 m were considered and compared against the UK Navy QinetiQ 90 tables for a similar estimate of probability of decompression sickness. RESULTS: The SQP method reliably produced schedules with fast and stable convergence to an optimized solution. Comparison of the optimized decompression schedules with the QinetiQ 90 schedules showed similar stop times for shallow dives to 18 m. For dives with a maximum depth of 39 m to 81 m, optimizing the decompression resulted in savings in decompression time of up to 30 min. CONCLUSIONS: This paper has shown that it is feasible to produce optimized iso-probabilistic decompression tables given a reliable risk model for decompression sickness and appropriate dive trials.     

Decompression: English tables

The formulation of decompression procedures has generally been based on the observation that divers can be decompressed without stoppages to surface, from steady-state exposures of about twice the atmospheric pressure. Because decompression sickness rarely develops from this "no-stop decompression", it has been assumed that no gas is liberated. It is therefore assumed, in the calculation of the majority of decompression tables, that using a 2:1 decompression ratio allows the additional gas load from the hyperbaric exposure to be transported to the lungs in solution. Ultrasonic scanning and Doppler techniques have shown that this is not the case. Decompression tables must therefore be formulated so as to take into account the presence of gas, the critical diameter of circulating bubbles and the inherent unsaturation introduced by oxygen.     

Multiple sclerosis presenting as neurological decompression sickness in a U.S. navy diver

A case of clinically definite multiple sclerosis presenting as neurological decompression sickness is presented. A 23-yr-old U.S. Navy diver experienced onset of hypesthesia of the left upper trunk approximately 19 h after making two SCUBA dives. She did not seek medical attention until 3 wk later, at which time she was diagnosed with possible neurological decompression sickness. She was treated with hyperbaric oxygen, but demonstrated no improvement. Further evaluation led to the diagnosis of multiple sclerosis. This case underscores the potential similarity in neurological presentation between multiple sclerosis and decompression sickness. The differential diagnosis of neurological decompression sickness, particularly in atypical cases, should include multiple sclerosis. The appropriateness of medically clearing multiple sclerosis patients for diving is discussed.     

USAF treatment table 8: treatment for altitude decompression sickness

INTRODUCTION: Altitude decompression sickness (DCS) has been treated with hyperbaric therapy since 1941. Treatment has essentially followed the diving DCS paradigm. Expanding space operations and higher flying, more remotely placed military aircraft have stimulated a re-examination of this paradigm. Can the oxygen and pressure-producing resources in these austere environs be reduced without sacrificing treatment efficacy? METHOD: A prospective series of 12 patients was treated with a new treatment table. USAF Treatment Table 8 (TT8) consists of 100% oxygen delivered at 2 ATA for four 30-min periods with intervening 10-min air breaks (a total oxygen dose of 2 h). Inclusion spanned 1985-1989. RESULTS: There were 10 patients who were treated 11 times for Type I altitude decompression sickness. Treatment was successful in 91%. There was one failure (a recurrence of elbow pain) requiring further therapy. Two patients were treated for Type II altitude decompression sickness. Treatment was successful in 50%. There was one failure (incomplete clearance of sensory deficits and weakness in the shoulder) requiring further therapy. CONCLUSION: Although TT8 had two failures, its successes suggest that a new protocol for the treatment of altitude decompression sickness is viable. In addition, its successes further suggest that a more extensive clinical trial is in order.     

The effect of exposure to 35,000 ft on incidence of altitude decompression sickness

INTRODUCTION: Exposure to 35,000 ft without preoxygenation (breathing 100% oxygen prior to decompression) can result in severe decompression sickness (DCS). Exercise while decompressed increases the incidence and severity of symptoms. Clarification of the level of activity vs. time to symptom onset is needed to refine recommendations for current operations requiring 35,000-ft exposures. Currently, the U.S. Air Force limits these operations to 30 min following 75 min of preoxygenation. The objective of this study was to determine the effect of exercise intensity on DCS incidence and severity at 35,000 ft. METHODS: Following 75 or 90 min of ground-level preoxygenation, 54 male and 38 female subjects were exposed to 35,000 ft for 3 h while performing strenuous exercise, mild exercise, or seated rest. The subjects were monitored for venous gas emboli (VGE) with an echo-imaging system and observed for signs and symptoms of DCS. RESULTS: Exposures involving strenuous and mild exercise resulted in higher incidence (p < 0.05) and earlier onset of symptoms (p < 0.05) of DCS than exposure at rest. Mild and strenuous exercise during exposure did not differ in incidence or rate of onset. Incidence at 30 min of exposure was 8% at rest and 23% while exercising. CONCLUSION: The results showed that current guidelines for 35,000-ft exposures keep DCS risk below 10% at rest. Exercise, even at mild levels, greatly increases the incidence and rate of onset of DCS.     

Pre-treatment with hyperbaric oxygenation reduces bubble formation and platelet activation

Abstract Bubble formation and platelet activation are major factors contributing to decompression sickness. We hypothesized that pretreatment with hyperbaric oxygen immediately before a dive may reduce bubble formation and platelet activation in humans. Five healthy volunteer subjects (1 female and 4 males; age, 33.6±2.9 years; height, 170±3 cm; weight, 71±8 kg, body mass index, 24.5±22.0 kg/m²) participated in this study with a 4-day protocol. On day 1, a multiplace hyperbaric chamber was used to compress all subjects with air to 4 atmosphere absolute (ATA) for 25 minutes; they were then decompressed to surface pressure at a rate of 10 m/min. Once surface pressure was reached, they were monitored with precordial ultrasonic Doppler at 20 min, 50 min and 80 min. Venous blood samples were obtained immediately before and after pressure exposure. On day 2, all subjects were compressed at 1.6 ATA for 45 min with 100% oxygen; they were then decompressed to surface pressure at a rate of 10 m/min. As soon as they reached surface pressure, they were immediately exposed to the same compression-decompression protocol as day 1; blood samples were taken after the second pressure exposure. Platelet activation was examined before and after exposure. On days 3 and 4, we inverted the protocol to minimize the influence of the first immersion on bubble formation. In comparison to the standard compression protocol, compression after hyperbaric oxygenation led to significantly reduced bubble numbers and platelet activation (11.4%±0.7% vs. 5.4%±0.5%, p<0.05). This study shows that hyperbaric oxygenation pretreatment significantly reduces decompression-induced bubble formation and platelet activation. Hyperbaric oxygenation pretreatment may reduce the risk of decompression sickness in at-risk activities.     

The treatment of decompression sickness

The initial event in decompression sickness is the separation of gas from solution because of supersaturation. If this event gives rise to immediate symptoms, recompression is remarkably effective. This end-point is characteristic of joint pain, that is, Type 1 decompression sickness. Unfortunately the onset of serious Type 2 decompression sickness may be insidious and the delay may be associated with blood-brain barrier dysfunction. Pressure is less effective in the resolution of this problem than a raised partial pressure of oxygen. Standard therapy using oxygen may be associated with worsening of symptoms and air tables with recurrence. Recompression to 4 ata and the use of a mixture of 50% oxygen and 50% helium offers a good working compromise in the treatment of both serious decompression sickness and gas embolism arising in air diving, avoiding the need for a differential diagnosis. Only oxygen or helium and oxygen mixtures should be used in the therapy of decompression sickness in helium and oxygen diving. When therapy has been delayed, intravenous fluids and steroids are important adjuncts.     

模拟飞机座舱迅速减压肺损伤动物模型的研究

目的 建立迅速减压肺损伤的动物模型,为研究迅速减压肺损伤提供平台. 方法 健康一级新西兰白兔30只,分为4组,放入迅速减压舱内,舱内压力在0.3 S内由53.3 kPa迅速降低至19.3 kPa,停留3～5 S后,在1 min内迅速将减压舱压力恢复至正常地面大气压力. 结果 随着与气管相联的排气装置排气口直径的减小,各组动物肺脏损伤逐渐加重,肺脏内减压峰值升高(F=129.987,P<0.01). 结论 该迅速减压动物模型能够模拟肺脏内不同的减压峰值,客观地体现胸廓及膈肌在飞机增压座舱发生高空迅速减压时对肺脏的保护作用,为深入研究迅速减压肺损伤以及探讨机体对减压峰值的耐限问题提供了可靠手段.     

Explosive decompression of subjects up to a 20,000-m altitude using a two-pressure flying suit.

The RSAF two-pressure flying suit system to protect the pilot at high altitude has been tested from different medical safety aspects. To secure adequate alveolar oxygen pressure, the suit admits up to 70 mm Hg (9.3 kPa) positive pressure breathing by counter-pressure against the thorax and by a 3.2 times higher pressure in the anti-G suit. After 1 h of oxygen breathing, subjects were exposed to explosive decompression from an altitude of 9,000 m to 17,500 or 20,000 m in 0.5 s in a hypobaric chamber. No symptoms of decompression sickness or of alveolar rupture with gas embolism to the central nervous system were seen. Pulmonary X-rays after the test did not reveal any signs of lung rupture with extrapulmonary gas leakage. With the precordial Doppler ultrasound technique, intracardial gas bubbles (silent bubbles) could be detected only in one subject after explosive decompression to a 20,000-m altitude in the 10 experiments.     

乙醇治疗急性脊髓型减压病的实验研究

目的 观察乙醇治疗大白兔急性脊髓型减压病的疗效.方法 将58只新西兰大白兔分为乙醇组25只、生理盐水组20只和不采取任何治疗措施的对照组13只.将乙醇组15只、生理盐水组8只、对照组8只兔分别放入动物舱内,在15 min内用压缩空气加压至0.6 MPa,停留60 min,然后用5min匀速减压至常压出舱,制成急性脊髓型减压病模型.乙醇组出舱后30 min用25％乙醇溶液(3ml/ks),由耳缘静脉缓慢注射入血管;生理盐水组注射(3 ml/kg)生理盐水;对照组不作任何处理.所有兔均在造模前和出舱3d后行Tarlov法评估后肢运动、做MRI及测量脊髓诱发电位,随后处死,解剖,观察腹腔脏器并取胸腰段脊髓行HE染色和光镜检.结果 (1)Tarlov评分:乙醇组(4.31±0.63)分,生理盐水组( 1.25±0.50)分(与乙醇组比较,P＜0.01);对照组(1.20±0.83)分(与乙醇组比较,P＜0.01).(2)MRI检查:乙醇组胸腰脊髓轻度肿胀,生理盐水组和对照组胸腰段脊髓肿胀,正常形态消失,并可见散在局灶性和弥漫性T2W高信号影.(3)SCEP检测:乙醇组的脊髓诱发电位N21潜伏期和波幅无明显变化,生理盐水组和对照组的脊髓诱发电位N21潜伏期较进舱前明显延长,差异有统计学意义(P＜0.01),波幅明显降低,差异有统计学意义(P＜0.01).(4)HE染色后,乙醇组光镜下仅见脊髓内少量散在出血及炎症细胞浸润;生理盐水组和对照组解剖可见尿潴留、肠胀气,光镜下可见脊髓弥漫出血、淤血、大量空泡及炎症细胞浸润.结论 乙醇有可能成为治疗急性脊髓型减压病的一种应急方法.     

Mechanical vs. ischemic mechanisms for decompression sickness.

We used 20 kangaroo rats to investigate the effect of exposure to low oxygen levels (0.11 Atm 02 inspired partial pressure) prior to decompression from a steady-state condition. This hypoxia was found to afford significant protection against limb bends as simulated in those animals by tail biting. Yet, it potentiated neurologic symptoms compared with a control exposure on air with the same level of nitrogen supersaturation. However the incidence of simulated limb bends in the same animals was the same with hypoxia as with another control exposure at a pressure estimated to give extravascular bubbles of the same size upon decompression. The results are, therefore, consistent with a simple mechanical basis for limb bends, but are difficult to explain by any ischemic mechanism since a general hypoxia exacerbates any pain produced by oxygen deficiency in the tissues. However, the reverse may be true for some forms of neurologic decompression sickness and the two such cases reported here are consistent with that view, although not statistically significant.     

兔实验性重型减压病时组织的病理变化

目的 探讨急性重型减压病时机体病理组织的系统性改变.方法 以新西兰大白兔为实验动物,用压缩空气在3 min内匀速加压至0.7 Mpa,停留60 min后,5 min内快速减压出舱,建立大白兔急性减压病模型.观察加压前、减压后生存率、减压病症状,并在减压后15 min、1 h、24 h取兔心、肝、肺、肾、脑等脏器组织,用甲醛溶液固定、石蜡包埋、切片、HE染色后观察病理变化.结果 肺、肝及脑的病理学改变较明显,肾、心的病理改变较轻.减压后15 min内死亡的兔以脑组织水肿为主;减压后有症状但存活1 h者以心脏病变为主;减压后24 h病理组织显示各脏器水肿、出血减少,以炎性浸润及微血栓形成为主.结论 脑的急性水肿是导致重型减压病急性死亡的主要原因;快速减压后1h内为抢救重型减压病的关键时期,该时期主要以循环系统的病变为主;减压后24 h主要以炎症浸润及微血栓形成为主.