加压治疗减压病机理的实验研究

目的探讨加压治疗减压病的机理。方法在兔减压病(decompression sickness,DCS)发病后和发展到严重DCS时,人随动物立即被加压到0．5MPa,在压力下Doppler连续监测心前区,间断显微球结膜血管,观察动物行为。结果加压的疗效、循环系统内气泡的消除与微血管功能恢复的速度、程度呈相应关系。血管功能严重障碍或衰竭的动物,在加压和减压过程中,因微血管功能进行性障碍,使病情恶化。结论压力只能消除DCS发病时血液中气体过饱和的膨胀力,使有代偿功能的痉挛血管解痉,恢复血液循环,逆转DCS的发病过程。压力不能使功能严重障碍、衰竭的血管恢复功能、不能修复损伤组织,也不能直接消除循环系统内的气泡。     

口服酒精溶液对豚鼠高空减压气泡生成的影响

目的为建立高空减压病易感性的筛选指标提供实验依据，我们观察了豚鼠口服酒精后高空减压时体内气泡生成的变化。方法30只豚鼠随机分成3组，其中两组分别在口服50％酒精溶液4.0和8．0ml后10.min和20min减压至13000m高度。用超声多普勒装置检测豚鼠心前区气泡音。结果口服8．0ml酒精溶液后减压，气泡生成明显增加（P＜0．01），血浆表面张力明显降低（＜0．01）。结论减压前饮酒能明显促进动物高空减压气泡的生成。     

减压病病因和发病机理的研究

目的探明减压病(DCS)病因,阐明发病机理。方法对暴露在高气压环境不充分减压的动物分别进行显微球结膜,麻醉、手术暴露股动脉测血压和病理学检查。结果减压后血管痉挛、功能障碍的动物都有DCS症状;血压升高期是严重DCS的发病阶段;DCS动物血管内皮肿胀、破裂、出血。结论DCS是因环境压力降低,血液中气体过饱和形成的膨胀力(病因)作用血管,使血管痉挛、功能障碍引起的疾病(发病机理)。     

循环系统内注入空气致病机理的探讨

为探讨循环系统内注入空气致病机理，向２２只狗大隐静脉注入不等量空气并在心前区用Ｄｏｐｐｌｅｒ监测心率，心律和气泡音。结果发现，维持心前区Ⅳ级气泡音的１７只狗，依次出现呼吸和心率加快，心律紊乱，心率缓慢，腹式呼吸加强，基中１２只狗继续缓慢注入空气至呼吸停止，任选１０只狗胸外按压，８只狗复苏后行为针异常，２只狗未能复活。另２只狗呼吸停止后立即尸检，可见右心房，室，腔静脉和肺血管中有大量气泡。提示：循环     

空气潜水作业实时安全减压理论研究

目的:建立实时减压方案的理论计算方法。方法:根据Haldane理论 [ 1] ,确定适合实时安全减压方案计算的假定时间单位、理论组织分类、氮过饱和安全系数及其选取方法,建立实时安全减压方案的计算方法;通过112只羊次,28个加压方案观察动物出舱后的行为学改变并检测多普勒气泡音。 结果:出舱后动物均未出现行为学异常,多普勒血流气泡音检测均为零级。结论:理论计算得到的减压方案安全可靠。     

自适应噪声相消法提取减压病气泡信号

在航空和潜水医学领域中,应用Doppler 超声监听心前区气泡音判断减压安全性和减压病严重程度是一种有效的方法。然而,至今国内外定量的气泡检测手段还没有得到解决。本文经过研究分析提出了自适应噪声相消法。本方法对抑制背景噪声提取气泡信号行之有效。信号处理后信噪比提高9dB。以该算法形成的计算机气泡检测系统可同时给出气泡计数、气泡能量密度波形以及心区信号的频谱直方图等信息。     

高空减压病研究工作的若干进展

对高空减压病加压治疗的新经验及减压气泡检测方法的新成就进行了综述，并对下述几种情况的处理提出了相应的建议：高空上升时在空中求发病；空中发病、下降至地面时症状已消除以及下降至地面后发病的病例。对体表心前区多普勒超声气泡检测的假阳性与假阴性问题，以及视觉辅助系统与计算机辅助系统在提高检测方法的敏感性与特异性方面的作用进行了讨论。     

高空减压气泡的多普勒超声检测

1968年，Spencer等以及Gillis等将多普勒(Doppler)超声血流测定技术加以改进，应用于高压一减压实验动物血管中气泡的检测以来，现已发展为广泛使用的无创性人体心前区气泡检测方法，成为潜水医学、航空航天医学中减压病的有效研究手段之一，并为该领域谱写了新篇章。我国海军医学研究所1975年首先开始应用Doppler超声技术于科研工作，也已获得一定成果。     

静脉注射钙镁离子对家兔高空减压血流中气泡生成的影响

观察了静脉注射硫酸镁和葡萄糖酸钙溶液对家兔高空减压时血流中气泡生成的影响。实验采用3×3拉丁方设计，共进行了4组，36次实验。硫酸镁溶液浓度为12.5％，葡萄糖酸钙浓度为7．5％。减压高度12000m，停留时间20min。用多普勒超声检测心前区血流中气泡。结果表明，注射硫酸镁和葡萄糖酸钙后气泡生成量和出现时间无明显变化。提示单纯血液镁、钙离子升高不是静脉气泡生成的易感因素。     

模拟高海拔氦氧常规潜水减压方案的计算和验证

目的 运用高海拔气压值与海平面气压值之比,计算高海拔氦氧常规潜水的减压方案,并在高低压舱内模拟高海拔氦氧常规潜水验证减压方案的安全性.方法 用高海拔气压值与海平面气压值的比率作为校正因子,对氦氧常规潜水减压表中各有关深度值进行修正后确定4个高海拔氦氧常规潜水减压方案.4名健康男性潜水员在高低压舱内分别暴露于海拔3000、4000和5200 m,进行了模拟30 m/60 min和50 m/60 min的氦氧常规潜水,减压过程中每隔1个停留站深度及返回高海拔压力时对潜水员进行舱内心前区多普勒超声气泡检测及录音.结果 静态、动态多普勒超声气泡检测均未发现血流气泡音,也未发现减压病症状和体征.结论 本研究确定的4个减压方案安全可行.     

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.     

The risk of altitude decompression sickness at 12,000 m and the effect of ascent rate

INTRODUCTION: Loss of aircraft cabin pressurization can result in very rapid decompression rates. The literature contains reports of increased or unchanged levels of altitude decompression sickness (DCS) resulting from increasing the rate of decompression. We conducted two prospective exposure profiles to quantify the DCS risk at 12,192 m (40,000 ft), and to determine if there was a greater DCS hazard associated with a much higher rate of decompression than typically used during past DCS studies. METHODS: The 63 human subjects participated in 80 altitude chamber decompression exposures to a simulated altitude of 12,192 m (2.72 psia; 18.75 kPa) for 90 min, following preoxygenation with 100% oxygen for 90 min. Half of the subject-exposures involved an 8-min decompression (1,524 mpm; 5,000 fpm) and the other half experienced a 30-s decompression (mean of 24,384 mpm; 80,000 fpm). Throughout each ascent and exposure, subjects were seated at rest and breathed 100% oxygen. At altitude, they were monitored for precordial venous gas emboli (VGE) and DCS symptoms. RESULTS: The higher decompression rate yielded 55.0% DCS and 72.5% VGE and the lower rate produced 47.5% DCS and 65.0% VGE. Chi square and log rank tests based on the Kaplan-Meier analyses indicated no difference in the incidence or onset rate of DCS or VGE observed during the two profiles. CONCLUSION: Decompression rate to altitude up to 24,384 mpm was found not to have an effect on DCS risk at altitude. However, research is needed to define the DCS risk with decompression rates greater than 24,384 mpm. It was also found that the onset time to DCS symptoms decreases as altitude increases.     

静脉注射全氟碳剂联合酒精湿化吸氧对兔减压病的影响

目的 观察静脉注射全氟碳剂(perfluorocarbon,PFC)联合酒精湿化吸氧对兔减压病发病率、病死率、红细胞和血小板计数的影响.方法 90只4月龄健康雄性新西兰大耳实验兔随机分为5组,包括正常对照组(NC组)、减压病(decompression sickness,DCS)建模组(DCS组)、减压病建模组+静脉注...     

Stress biomarkers in a rat model of decompression sickness

INTRODUCTION: Immune reactivity, stress responses, and inflammatory reactions may all contribute to pathogenic mechanisms associated with decompression sickness (DCS). Currently, there are no biomarkers for DCS. This research examined if DCS is associated with increased levels of biomarkers associated with vascular function, early/non-specific stress responses, and hypothalamic-pituitary-adrenal (HPA) axis stress responses. METHODS: Rats undergoing a test dive to 175 ft of seawater (fsw) (6.2 ATA) for 60 min with a rapid decompression were observed for DCS (ambulatory deficit). Animals exercised on a rotating cage (approximately 3 m x min(-1)) throughout the dive and subsequent 30-min observation period. All animals were euthanized and blood and tissue samples (brain, liver, lung) were collected for analysis of CRP and ET-1 by ELISA and stress markers by PCR. RESULTS: HO-1 and HSP-70 increased in the brain, and HO-1, Egr-1, and iNOS increased in the lungs of animals with DCS. There was no difference in any stress marker in the liver, or in serum levels of CRP or ET-1. CONCLUSIONS: The results demonstrate that < 30 min after surfacing, there are genomic changes in animals with DCS compared with animals not showing signs of DCS. Identification of specific markers of DCS may permit use of such biomarkers as predictors of DCS susceptibility and/or occurrence.     

Field trials of no-decompression stop limits for diving at 3500 m

INTRODUCTION: In 1990, Bo?azi?i University (Istanbul, Turkey) launched an altitude diving program to develop techniques and safe decompression profiles for diving at high terrestrial altitudes. Following pioneering diving expeditions to lakes at high elevations in 1990-1992, it was deemed necessary to calculate new tables. METHODS: Bottom time limits for dives requiring no decompression stops (no-d) were calculated for 3500 m using linear extrapolation of U.S. Navy M-values decreased by 4 ft of sea water (M4 limits). These limits were tested for 15, 18, 21, 24, 27, and 30 m of depth by diving in the Great Sea Lake at Mt Ka?kar (3412 m) with 10 dives per profile. RESULTS: The mean decompression sickness (DCS) risk estimated from precordial bubble scores (Spencer Scale) ranged from 0.3% to 2.8% per profile. After three expeditions, 165 dives had been achieved with a cumulative bottom time of 3199 min. No DCS occurred in dives that adhered to the M4 no-d limits. However, two cases of Type I and one case of Type II DCS were encountered where the divers accidentally exceeded those limits. DISCUSSION: Considering the estimated risk of DCS and the relatively small number of trials, a more conservative approach was used to develop a final set of high altitude dive tables. This conclusive approach used continuous compartment half-lives. It is based on fitting a surface of allowable supersaturation limits using the empirical M-values from existing tables as well as our altitude diving data, together with an added constraint that forces calculated M-values to stay below the available M-value data.     

Twenty years of treating decompression sickness

Twenty years of treatment records were searched for cases of serious decompression sickness (DCS). Spinal cord DCS was the most common presentation. The efficacy of various treatment tables were compared. Oxygen tables were found to be as effective as long air tables in treating cases presenting within 12 h of the onset of symptoms and were superior for cases presenting later. Using RN 61 (USN 5) to treat serious decompression sickness resulted in a high post-treatment relapse rate. Other inappropriate practices such as in-water air treatment and nontreatment of spontaneously recovering cases resulted in a high incidence of deterioration or relapse.     

大鼠减压应激损伤时脑和肝胞液糖皮质激素受体的改变

目的 探讨大鼠减压应激损伤时大脑和肝脏胞液糖皮质激素受体结合量的变化。方法 大鼠３０只,随机分为５组,置于加压舱内,进行加减压实验。出舱后,以＾３Ｈ地塞米松为配体,测定了动物脑、肝胞液糖皮质激素受体亘的改变,同时还监测了动物心前区域压气泡的变化。结果 减压应激损伤后,动物肝、脑胞液糖皮质激素受体结合量的下降,尤其以脑胞液中糖皮质激素受体减少为明显（Ｐ〈０．０１,Ｐ〈０．０５）。实验还观测到,减压后     

Treatment of decompression sickness in swine with intravenous perfluorocarbon emulsion

BACKGROUND: We examined an adjunctive treatment for severe decompression sickness (DCS) to be used when hyperbaric treatment is delayed or unavailable. HYPOTHESIS: It has been hypothesized that intravenous perfluorocarbon (PFC) emulsion combined with 100% inspired O2 would improve the outcome in severe DCS. METHODS: Swine (n = 45) were compressed to 4.9 ATA on air for 22 h and brought directly to 1 ATA at 0.9 ATA min(-1). The animals were then randomized to three groups. The first group breathed ambient air, the second group breathed 100% O2, and a third group received 6 ml x kg(-1) of perflubron emulsion (Oxygent) intravenously and breathed 100% O2. Outcomes of neurological and cardiopulmonary DCS and death were recorded. RESULTS: Animals that received PFC emulsion sustained less DCS (p < 0.01) than the other groups (53% vs. 93%). No animals in the PFC group sustained neurological DCS, which was present in 69% of the subjects in the other two groups. CONCLUSION: O2 breathing postdive did not significantly reduce morbidity or mortality in this model. Postdive treatment with PFC emulsion and 100% O2 decreased the incidence of DCS after nonstop decompression from saturation.