高压氧对实验性减压病兔肺间质细胞增生的影响

目的 探讨高压氧(HBO)对实验性减压病兔肺间质细胞增生的影响.方法 将38只实验兔放入加压舱中,于5 min内用压缩空气加压至0.6 MPa,停留60 min,然后于3～5 min内减至常压.HBO-1次组出舱后1 h接受HBO治疗1次,HBO-4次组出舱后1 h至3 d每天接受HBO治疗1次(0.25 MPa),共4次;减压病对照组:出舱1 h至3 d,每天暴露舱内常压空气1次,共4次;常氧高压氮组:出舱1 h至3 d,每天暴露常氧高压氮1次(0.25 MPa),共4次;健康对照组:暴露于常压空气中常规饲养3 d,无特殊处理.结果(1)减压病兔组肺间质细胞增生标记指数明显高于空白对照组(P<0.01);(2)HBO-1次组肺间质细胞增生标记指数高于HBO-4次组(P<0.05);(3)减压病兔HBO-1次和HBO-4次组肺间质细胞增生标记指数低于减压病对照组及常氧高压氮组(P<0.05).结论(1)快速减压可造成急性肺损伤,表现为肺间质细胞增生;(2)HBO对减压病兔的肺间质细胞增生有抑制作用,从而促进急性肺损伤后的修复,且多次HBO治疗疗效优于单次治疗.     

氦氧潜水减压病二例

在 1 999年 8月我部组织帮司 80 m氦氧潜水训练中 ,出现两例轻型减压病 ,报告如下。例 1　男 ,2 6岁 ,潜水年限 7年。下潜深度 78m,水下工作时间 30 m in,采用前苏联氦氧重潜水减压表 80 m 30 min方案减压。出舱后一般情况好 ,自行去 2楼甲板做心电图检查、3楼甲板做肺功能测试。出舱后 5 0 min诉两膝关节疼痛 ,检查一般情况好 ,两膝关节无红肿 ,无明显压痛点 ,拟诊“减压病”。采用美国海军减压病加压治疗表 ,吸氧加压至 1 80k Pa,症状好转 ,在该压力下停留 8min症状消失 ,为此确诊为轻型减压病 ,用治疗方案 V减压出舱。症状无复发 ,治愈…     

加压治疗陪护人员出舱后发生轻型减压病一例

患者 ,男性 ,38岁 ,潜水工龄 2 0年。2 0 0 1年 2月 2 4日 11∶ 37时 ,在某大坝 ,为援救 1名潜水 5 8m、水下工作 13min,未经水下停留减压直接上升出水的潜水员进行预防性加压治疗而陪舱加压。按照海军医学研究所制定的“空气潜水减压病加压治疗表” 氧方案 ,即 70 0 k Pa(表压 ,下同 )、30 min吸氧方案 ,治疗总时间 473m in。出舱后 30 min,患者自觉双上肢皮肤瘙痒 ,左肩关节疼痛 ,洗热水浴后未见好转 ,且左肩关节疼痛逐渐加重。自诉在陪舱减压过程中 ,很少吸氧 ,且因过度疲劳而长时间睡觉。诊断为急性轻型减压病。 5 0 min后 ,再次进舱加…     

高压氧治疗后发生减压病三例

我院 1 998年收治 3例因高压氧 (HBO)治疗中减压不当而反复发生减压病的患者 ,均获痊愈。现将治疗中的一些体会报告如下。3例均为女性 ,年龄 38～ 5 2岁 ,分别因左股骨颈骨折内固定术后、颈椎病引起双手麻木和腰椎骨折伴左下肢功能障碍在某医院接受 HBO治疗。HBO治疗压力 0 .2 5 MPa(绝对压 ,下同 ) ,加压时间 2 0 m in,压力下吸氧 30 min 2次 ,中间呼吸空气 1 0 min。减压采用空气阶段等速减压法 ,根据患者陈述 ,减压时间一般不超过 2 0 min,开始阶段较慢 ,后半阶段较快。每日 HBO治疗 1次。3例患者自诉多次在出舱后觉皮肤搔痒及关节…     

高压氧对实验性减压病兔脊髓诱发电位的影响

目的　探讨实验性减压病兔脊髓诱发电位的改变及高压氧 (HBO)对其影响。方法　将 3 2只实验兔放入加压舱中 ,于 5min内用压缩空气加压至 0 .6MPa,停留 60 min ,然后于 3～ 5m in内减至常压。分别于进舱前、出舱后 3 h和 3 d,进行脊髓诱发电位检查。 HBO组 :出舱后 1 h至 3 d,每天接受HBO治疗 1次 (0 .2 5MPa) ;常氧高压氮组 :出舱后 1 h至 3 d,每天暴露常氧高压氮 1次 (0 .2 5MPa) ;对照组 :出舱 1 h至 3 d,每天暴露舱内常压空气 1次。结果　 (1 )三组家兔减压后 3 h脊髓诱发电位 N2 1潜伏期均较进舱前延长 (P<0 .0 1 )、波幅有降低趋势 (P<0 .0 5) ;(2 ) HBO和常氧高压氮可使 N2 1潜伏期缩短 (P<0 .0 1 ) ,波幅增高 (P<0 .0 5)。结论　 (1 )快速减压可造成家兔减压病脊髓损伤 ,表现脊髓诱发电位 N2 1改变 ;(2 ) HBO和常氧高压氮对减压病脊髓损伤均有治疗作用 ,但 HBO疗效优于常氧高压氮     

高压氧联合用药综合治疗视神经损伤疗效观察

目的:观察高压氧(HBO)联合用药综合治疗视神经损伤的临床疗效.方法:在常规治疗基础上加用HBO治疗,采用空气加压舱,治疗压力0.2 MPa,使用微阻力面罩供氧,一般加压、减压时间20～30 min,稳压70 min,吸纯氧60 min,中间休息10 min,1次/d,10次为1疗程,本组病人HBO连续治疗3个疗程.对照组:除不用HBO治疗外,使用药物与HBO组相同,连续治疗30 d.结果:HBO组治愈18例, 有效36例,无效5例;对照组治愈9例, 有效15例,无效9例.疗效显著, P＜0.05.结论:HBO治疗结果表明,HBO联合用药治疗,能够达到协同作用,增进疗效的目的.     

高空迅速减压飞行人员的临床诊治和医学鉴定

目的 探讨飞行中高空迅速减压飞行人员的临床诊治经验和医学鉴定方法。方法 回顾分析近10年来空军发生的5起19人次高空迅速减压病例资料,暴露高度为8300至10 000 m. 结果 ①5起高空迅速减压中有3起10人（A组）返航后未经休息吸氧和高压氧治疗,其中7人发生了Ⅱ型高空减压病,发病率为70%,另2起9人（B组）返航后及时休息吸氧并送就近医院作高压氧治疗,均未发生高空减压病,两组高空减压病发生率有显著性差异（P〈0.01）.②两组对比分析发现,除了已明确的迅速减压时的高度外,在本组资料中个体敏感性、减压后高空缺氧以及空中和返航后的处置是否得当是影响发病的重要因素.③所有发病者经治疗均重返飞行岗位,但发病后治疗不适当或飞行员出现心理障碍会延长康复时间。 结论 高空迅速减压可对飞行人员造成显著的心理和生理影响,并且发生高空减压病的危险很大,减压后空中及返航后处置是否得当是影响病情发展的重要因素。     

高压氧治疗中小儿发生支气管痉挛九例

我院自 1995年 1月～ 1999年 11月 ,在利用高压氧(HBO)治疗小儿相关疾病时 ,发生了支气管痉挛 9例 ,现报道如下。一、临床资料9例患者均为本院病例 ,年龄最大 8岁 ,最小 8个月 ,平均 4.6岁 ;男性 8例 ,女性 1例 ;脑性瘫痪 4例 ,颅脑损伤 5例。 HBO治疗 :采用大型加压舱 ,先用压缩空气向舱内加压使舱内压力达 0 .2 MPa(绝对压 )后稳压 ,然后在供氧压力为0 .6 MPa下 ,采用浙江梅城电化分析仪器厂提供的胶管吸排氧装置戴面罩吸纯氧 80 m in,中间休息 10 min吸舱内空气 ,吸氧完毕后减压出舱 ,每日 1次。临床药物治疗 :9例患者在HBO治疗前…     

高压氧在加、稳压不同阶段吸氧对治疗脑血栓形成疗效的影响

目的探讨高压氧在加、稳压不同阶段吸氧对治疗脑血栓形成的临床疗效和疗程选择。方法将80例脑血栓形成患者按加、稳压阶段吸氧的高压氧治疗分为两组,两组均配合药物治疗。观察组50例在加压阶段就开始吸氧气,对照组30例在加压阶段吸空气,稳压阶段吸氧气。结果观察组50例治愈和显效率为94%,对照组为56.6%,观察组疗效明显高于对照组(P<0.05)。结论加压阶段吸氧治疗脑血栓形成能提高疗效。第2～3疗程效果最佳。     

空气常规潜水减压病辅助治疗的某些进展

空气常规潜水减压病 (简称 DCS)的病源性根治疗法仍是加压治疗 (包括吸氧和不吸氧方案 )。事实上 ,DCS单靠加压治疗并不一定都能治愈。有资料统计 [1 ] ,经再加压和高压氧 (HBO)治疗后 ,约 1/3潜水员仍遗留症状。要取得满意疗效 ,辅助疗法配合得是否恰当 ,有时显得尤为重要。本文将近年来 DCS辅助治疗的某些进展综述如下。一、DCS辅助治疗的现状DCS辅助治疗包括 :氧疗、补液、糖皮质激素、抗凝剂和降温疗法。1.氧疗 :吸氧可降低肺泡气中氮分压 ,加大组织和肺泡间氮气的压差梯度 ,促进氮的脱饱和。对 DCS的组织缺氧也需及时尽早供氧…     

高压氧对实验性减压病兔脊髓bFGF表达的影响

目的探讨实验性减压病兔脊髓bFGF的改变及高压氧对其影响。方法实验家兔随机分为7组：正常组、减压病3h组、减压病3d组、高压氧3h组、高压氧3d组、常氧高压氮3h组、常氧高压氮3d组。采用快速减压方法制备减压病模型，用免疫组织化学方法检测胸髓及腰髓中bFGF表达。结果（1）快速减压后各组bFGF表达均较正常组增加（P〈0．01），3h组之间无差异（P〉0．05）；（2）减压病3d组较3h组bFGF表达显著增高（P〈0．01），高压氧3d组较3h组显著降低（P〈0．01），常氧高压氮3d组较3h组有所降低（P〈0．05）；（3）高压氧3d组与常氧高压氮3d组均较减压病3d组显著降低（P〈0．01），高压氧3d组较常氧高压氮3d组降低（P〈0．05）。结论减压病脊髓损伤后bFGF表达增加；高压氧和常氧高压氮对减压病脊髓损伤起保护作用，高压氧效果优于常氧高压氮。     

高压氧下大鼠脑组织中氧化氮合酶阳性细胞的表达(论著)

目的：探讨高压氧（HBO）对视觉中枢的影响。方法：SD大鼠12只，随机分为3组：分别为常压对照组（NP组），高压空气对照组（HBA组），和HBO实验组（HBO组）。HBA组和HBO组动物分别给予0．25MPa高压空气和纯氧，升压20分钟，在0．25MPa下稳压4小时，然后经20分钟减至常压。动物出舱后立即灌注取脑，利用NADPH-黄递酶（NADPH-diaphorase）组织化学方法，观察氧化氮合酶（NOS）阳性细胞见脑组织外侧膝状体（LGN）、视皮层及大脑顶叶皮层的表达。结果：NOS阳性细胞存在于大鼠LGN、视皮层及大脑项叶皮层中。在0．25MPaHBO作用下，视皮层、大脑顶叶皮层中NOS阳性细胞明显增加（P＜0．05），而LGN与对照组相比无显著性差异（P＞0．05）。结论：HBO对视觉中枢的毒性作用与视皮层NOS阳性细胞增加密切相关。     

Prophylactic high dose methylprednisolone fails to treat severe decompression sickness in swine

INTRODUCTION: Controlled decompression from saturation conditions is not always an option, particularly in a disabled submarine scenario. Hypothesis Prophylactic high dose methylprednisolone (MP) would improve outcome in severe cases of decompression sickness (DCS). METHODS: Littermate pairs of male Yorkshire swine (n = 86, mean weight +/- SE = 19.3 +/- 0.2 kg) were randomized to one of three groups, then compressed on air to 4.3 ATA (33 msw) for 22 h and brought directly to surface pressure (1 ATA) at 0.9 ATA x min(-1). The MP-50 group received i.v. infusion of 50 mg x kg(-1) of MP dissolved in 60 cc normal saline (NS) immediately prior to the hyperbaric exposure. The NS group received 60 cc NS i.v. immediately prior to the hyperbaric exposure. The MP-10 group received i.v. infusion of 10 mg x kg(-1) MP dissolved in 60 cc NS during the hyperbaric exposure, 7 h before the decompression. RESULTS: Outcomes of severe DCS and death were recorded. NS group: 14 DCS, 4 died; MP-50 group: 19 DCS, 12 died; MP-10 group: 19 DCS, 10 died. Compared with the NS group, logistic regression analysis suggested that animals in the MP-10 group were more likely to get severe DCS and to die (p < 0.01) and animals in the MP-50 group were more likely to die from their disease (p < 0.01). DISCUSSION: Prophylactic high dose MP exerts no protective effect against severe DCS and actually worsens mortality in this model. An earlier group of untreated controls (UC, n = 44, 30 DCS, 11 died, mean weight +/- SE = 19.9 +/- 0.3 kg) exposed to the same profile was also available for analysis. Comparison of the UC and NS animals suggested that pre-dive NS treatment may protect against severe DCS.     

Altitude decompression sickness symptom resolution during descent to ground level

INTRODUCTION: Altitude decompression sickness (DCS) is a health risk associated with the conduct of high altitude airdrop operations, high altitude reconnaissance, future fighter operations, hypobaric chamber training, unpressurized flight, and extravehicular activity (EVA) in space. The treatment for DCS includes the provision of 100% oxygen (O2) at ground level (GLO) and/or hyperbaric oxygen therapy (HBO). In this paper we examine the effect of repressurization to ground level from hypobaric conditions on DCS symptoms. Timely recompression (descent at first recognition of any DCS symptom) may be a safe, effective treatment for the large majority of DCS symptoms. METHODS: Data from altitude chamber exposures recorded in the Air Force Research Laboratory (AFRL) Altitude DCS Database were reviewed to determine the level of recompression required for complete resolution of 1,699 observed symptoms. RESULTS: Of the 1,699 DCS symptoms reviewed, 66 (3.9%) resolved at altitude, 117 (6.9%) resolved at ground level, and 1,433 (84.3%) resolved during descent. Increasing the pressure by 138 mmHg from the altitude of exposure where symptoms occurred resolved roughly 50% of symptoms. Little resolution of symptoms was noted with recompressions of < 50 mmHg. The greatest rate of symptom resolution occurred with recompressions of 50-250 mmHg. CONCLUSION: These findings support the concept that descent and postflight, ground-level oxygen may be sufficient to relieve the majority of altitude DCS symptoms. HBO may be reserved for serious, recurring, delayed, or refractory symptoms. The findings also suggest a need for further study of DCS symptom resolution.     

Recompression during decompression and effects on bubble formation in the pig

INTRODUCTION: There is a relationship between gas bubble formation in the vascular system and serious decompression sickness. Hence, control of the formation of vascular bubbles should allow safer decompression procedures. METHODS: There were 12 pigs that were randomly divided into an experimental group (EXP) and a control group (CTR) of 6 animals each. The pigs were compressed to 500 kPa (5 ATA) in a dry hyperbaric chamber and held for 90 min bottom time breathing air. CTR animals were decompressed according to a modified USN dive profile requiring four stops. EXP followed the same profile except that a 5-min recompression of 50 kPa (0.5 ATA) was added at the end of each of the last three decompression stops before ascending to the next stop depth. RESULTS: All CTR animals developed bubbles, compared with only one animal in EXP. The number of bubbles detected during and after the dive was 0.02 +/- 0.02 bubbles x cm(-2) in CTR, while the number of bubbles detected in EXP were 0.0009 +/- 0.005 bubbles x cm(-2); the difference was highly significant. CONCLUSION: By brief recompression during late decompression stops, the amount of bubbles was reduced. Our findings give further support for a gas phase model of decompression.     

静脉注射全氟化碳乳剂对大鼠减压病防治作用的研究

目的 观察静脉注射全氟化碳乳剂(perfluorocarbon emulsion,PFCE)对大鼠减压病(decompression sickness,DCS)的防治作用.方法 以"700 kPa-60 min空气暴露、3 min减压"方案制备SD大鼠减压病模型,在高气压暴露前或暴露后即刻静脉注射PFCE(7 ml/kg),观察大鼠行为学(包括发病和死亡)以及肺、大脑和脊髓组织的病理变化.高气压暴露后以生理盐水处理,或者不经任何处理作为对照.结果 高气压暴露后即刻静脉注射PFCE的动物发病率(21.7%)显著低于生理盐水组(60.0%)(P<0.05)和空白对照组(66.7%)(P<0.01),死亡率(13.0%)显著低于空白对照组(42.9%)(P<0.05);大部分行为学及病理学指标显著改善(P<0.05).高气压暴露前静脉注射PFCE的动物发病率(80.0%)和死亡率(45.0%)与生理盐水组、空白对照组相比差异无统计学意义.结论 高气压暴露后即刻静脉注射PFCE对大鼠急性DCS具有良好的防治作用.     

不同高压氧治疗方案对急性一氧化碳中毒受损心肌的疗效分析

目的 探讨不同高压氧(hyperbaric oxygen,HBO)治疗方案对急性一氧化碳(carbon monoxide,CO)中毒受损心肌的影响.方法 对2006年10月至2010年3月收治的155例重症CO中毒患者进行HBO常规治疗(常规组,75例)和HBO改进治疗(改进组,80例).(1)常规组治疗方案:治疗压力0.25 MPa,加压20 min,稳压后吸氧2次,每次30 min,中间间歇10 min,减压20 min出舱.每日1次,12次为1个疗程,治疗9-68次.(2)改进组方案:前5 d采用HBO常规治疗,以后采用减小治疗压力、缩短吸氧时间、增加吸氧间隔、间歇给氧的治疗方案,治疗压力0.20 MPa,稳压吸氧4次,每次10min,中间间歇5 min,减压20 min出舱.连续治疗3 d后间隔1 d,10 d为1个疗程.2组患者使用相同的药物治疗方案.统计分析常规组和改进组ST-T变化及血清心肌酶变化.结果 改进组与常规组相比ST-T恢复率(56%,28%)明显升高(P＜0.05),HBO治疗第3天和第6天ST-T加重率(第3天21%、25%.第6天16%、27%)明显降低(P＜0.01);2组血清心肌酶恢复率和加重率比较差异有统计学意义(P＜0.05.P＜0.01).结论 HBO改进方案对CO中毒患者受损心肌疗效较好.

Abstract：

Objective To investigate the effects of different hyperbaric oxygen ( HBO) treatment profiles on damaged myocardium induced by acute carbon monoxide poisoning. Methods One hundred and fifty-five serious cases of acute carbon monoxide ( CO) poisoning admitted into the hospital for treatment from October 2006 to March 2010 were randomly divided into the routine HBO treatment group (the routine group,75 cases) and the improved HBO treatment group (the improved group,80 cases). The treatment profile of the routine HBO treatment group: the patients were compressed for 20 min to the treatment pressure of 0.25 Mpa. Following stabilization at the said pressure, the patients breathed oxygen twice for 30 min plus 10 min, once a day. The whole treatment course consisted of 12 sessions, with the patients receiving HBO treatments from 9 to 68 times. The treatment profile of the improved HBO treatment group: the patients were given routine HBO treatment in the first 5 days, then, received improved HBO treatment, with a treatment profile of lower pressure (0.20 Mpa) , shorter oxygen-breathing time, lengthening of oxygen-breathing intervals and intermittent oxygen breathing. Total oxygen-breathing time was 4 times, each for 10 min plus 3 times each for 5 min. Then, the patients were decompressed to the surface following 20-min oxygen-breathing decompression. The patients received treatment for a succession of 3 days, then, had 1-day interval, and the whole treatment course consisted of 10 sessions. Changes in ST-T and myocardial enzymes of both the routine HBO treatment group and the improved HBO treatment group were measured and analyzed. Results ST-T recovery rate of the improved HBO treatment group increased (56% ,28% ) obviously, when compared with that of the routine HBO treatment group(P ＜ 0. 05). ST-T worse rate decreased significantly following HBO treatment on the 3rd and 6th days (21% and 25% on the 3rd day, 16% and 27% on the 6th day) respectively (P＜0.01). Statistical differences could be seen in the myocardial recovery rate and worse rate, when a comparison was made between them (P＜0. 05, P＜0. 01). Conclusions The improved HBO treatment profile showed better therapeutic effect on damaged myocardium induced by CO poisoning. This treatment profile should be used instead of other treatment profiles.     

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.     

高压氧治疗对急性减压病患者外周血肿瘤坏死因子α、白细胞介素-6的影响

目的探讨高压氧治疗对急性减压病患者外周血肿瘤坏死因子α(TNF-α)和白细胞介素-6(IL-6)水平的影响。方法选取急性减压病患者30例,接受高压氧治疗,分别在治疗前,首次治疗结束即刻,治疗后第1、3、7天检测外周血TNF-α、IL-6水平。结果与治疗前比较,TNF-α水平在治疗后第1、3、7天明显下降;IL-6水平在治疗后第3、7天显著下降。结论高压氧治疗可以减少急性减压病患者外周血TNF-α、IL-6水平。