超声测量技术用于兔皮肤内高空减压气泡测量的探讨CSCD

目的：针对高空减压病病因学气泡生成的机制,探讨了用皮肤超声测量技术检测兔皮肤内减压气泡生成的可行性。方法测量者上升前呼吸纯氧排氮15 min后和家兔一起以30～50 m／s的速度上升到8000 m。在停留5 min和10 min时分别对家兔腹部皮肤进行超声测量,每个部位重复测量10次。测量仪器为德国MINHORST GobH公司生产的Collagenoson‐ICU皮肤高频回声断层扫描仪,其发射频率为22 M Hz ,探测孔径2 mm ,探测深度15 mm ,测量分辨率为0．15 mm。结果高空减压后,兔皮肤扫描图像中代表存在气体界面反射的明亮像素增多,减压前后的像素均值差异有统计学意义（ F＝11．162, P＜0．01）;减压后的像素值明显高于减压前（ P＜0．01）。结论本研究初步证明皮肤超声测量可望为减压病气泡生成的客观检测提供一个新的潜在指标。     

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。     

+Gz暴露对大鼠记忆功能和行为的影响

目的 探讨不同水平 Gz暴露对大鼠记忆功能和行为的影响。方法 24只雄性SD大鼠随机分为对照组、 6Gz组和 10Gz组3组，每组8只。 Gz暴露大鼠分别进行 6Gz／3min和 10Gz／3min暴露，记录 Gz暴露后不同时间大鼠记忆功能和行为的变化。结果 与对照组比较， 10Gz组大鼠反应时在 Gz暴露后即刻和2d时显著延长(P＜0．01)，错误次数及错误时间在 Gz暴露后6h时显著增加(P＜0．01)，中央格内停留时间在 Gz暴露后即刻、6h和ld时显著延长(P＜0．01)，站立次数和跨格次数则在 Gz暴露后即刻和2d时显著减少(P＜0．01)；而 6Gz组大鼠仅站立次数在 Gz暴露后即刻和2d时较对照组显著减少(P＜0．01)，其余指标均无显著性差异。结论 10Gz／3min暴露可引起暂时性大鼠记忆功能降低和行为改变。     

亚硒酸钠VE对奶牛生产性能的影响

试验采用对比试验设计,试验组与对照组妊娠母牛各为30头,在预产期前60－70d肌注亚硒酸钠VE50ml／头,出生犊牛再肌注5ml／头。结果表明,处理组母牛产后胎衣滞留率和发烧头数均低于对照组（P＜0．05）,而产后60d日产奶量却极显著高于对照组（P＜0．01）;处理组犊牛的初生重及60日龄个体日增重也极显著高于对照组（P＜0．01）,但其发病率和死亡率显著低于对照组（P＜0．05）。     

高压氧对快速减压致中枢神经损伤诱发神经元凋亡的效用

目的研究成年大鼠快速减压致中枢神经系统（CNS）损伤后神经组织细胞凋亡的变化及高压氧（HBO）暴露的效用。方法SD大鼠40只，按随机数字法分为10组，每组4只，即正常对照组、安全减压组、快速减压4个组（1．0MPa暴露5．5min后快速（50S）减至常压后6，24，48，72h组）、HBO4个组（快速减压后5h给予0．25MPa HBO暴露60min）。大鼠均分别于快速减压后6，24，48和72h同期取大脑，用原位末端TUNEL法标记凋亡细胞，光学显微镜下观察形态学改变和高倍镜计数阳性细胞计算凋亡指数。结果正常对照组和安全减压组未标记出TUNEL阳性细胞；快速减压致伤动物6h组CNS组织内仅见少量散在阳性细胞；24h组凋亡指数较6h组增加（P〈0．01）；48和72h组明显增加，达到高峰（P〈0．01）；TUNEL阳性凋亡细胞主要为神经元细胞。HBO暴露组24h组神经元凋亡指数明显较快速减压组相同时间组降低（P〈0．05），48h和72h组降低更加显著（P〈0．01）。结论神经元凋亡是快速减压致CNS损伤中神经元丧失的重要形式之一：HBO暴露能够减少损伤后期的神经元凋亡，对保存神经元、改善预后起到重要作用。     

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。     

模拟失重对流体剪切应力诱导成骨细胞环氧合酶-2表达的影响

目的 探讨模拟失重对成骨细胞力学信号转导功能的影响。方法 体外传代培养的大鼠乳鼠颅骨成骨细胞分为两组，一组置于回转器中培养，另一组则在地面重力环境下培养，60h后，将成骨细胞置于流室系统中进行刺激实验。流体剪切应力（FSS）分别为0．5Pa和1．5Pa，作用时间分别为30min和60min。其后进行免疫组化染色和图像分析。结果 在1G组，相同时间不同水平FSS作用诱导的环氧合酶－2（COX－2）蛋白表达无显著差异，FSS作用30min与60min所诱导的COX－2蛋白表达差异有显著性意义（P＜0．01）；模拟失重环境下COX－2蛋白表达发生下调性变化，仅在1．5Pa FSS作用60min的成骨细胞中检测到蛋白表达。相同时间和FSS下，模拟失重组与1G组COX－2蛋白表达水平的差异有显著性意义（P＜0．01）。结论 模拟失重时成骨细胞撂学信号转导功能发生了显著的下调性改变。     

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10000m。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、吸氧并送就近医院行高压氧治疗，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莺要因素。     

急性低气压缺氧对人体球结膜微循环的影响

对14名健康飞行员在低压舱以35m／s的上升速度上升至5000m高度，不吸氧，停留30min，用锦州光学仪器厂生产的XOX－IA型微循环显微镜放大40－100倍，进行了球结膜微循环的动态观察。结果表明，随着缺氧时间的延长，球结膜微循环形态、流态、总积分值明显增加（＜0．01），管袢分值无明显改变（P＞0．05）。细静脉扩张、微血管数减少明显（P＜0．01），细动脉无明显改变（P＞0.05）。下降地面后，各项指标基本恢复。提示，这些改变提高了血管的顺应性及心脏的功能。     

高压氧对荷S-180瘤细胞小鼠血液某些指标的影响(论著)

目的：探讨高压氧（HBO）暴露对荷瘤小鼠血液指标的影响。方法：用雄性Balb／C／小鼠20只，随机分成4组，每组5只。A组为正常对照；B组只行HBO暴露；C组只做肿瘤接种；D组行HBO暴露并接种肿瘤。B、D组经压力0．2MPa、氧浓度87％、氧分压0．174MPa的HBO暴露20次后，所有鼠摘眼球取血对其血红蛋白、白细胞总数、中性白细胞数、淋巴细胞数、中性白细胞百分比、淋巴细胞百分比作了观察。结果：（1）血红蛋白在HBO肿瘤组比单纯HBO组高（P＜0．01）；（2）白细胞总数在HBO肿瘤组分别高于对照组（P＜0．05）、单纯HBO组（P＜0．01）和单纯肿瘤组（P＜0．05）；（3）中性白细胞数在HBO肿瘤组和单纯肿瘤组，均比对照组高（P＜0．01，P＜0．05），而HBO肿瘤组分别比单纯HBO组和单纯肿瘤组高（P＜0．01，P＜0．05）；（4）淋巴细胞数各组之间均无明显差异；（5）中性白细胞百分比在HBO肿瘤组和单纯肿瘤组，均比对照组高（P＜0．01，P＜0．05），而HBO肿瘤组比单纯HBO组高（P＜0．01）；（6）淋巴细胞百分比在对照组分别比HBO肿瘤组和单纯肿瘤组高（P＜0．01，P＜0．05），而单纯HBO组比HBO肿瘤组高（P＜0．01）。结论：（1）HBO（氧分压＝0．174MPa）可使荷瘤小鼠的白细胞总数和中性白细胞数量提高，但未能改变正常     

The effect of staged decompression while breathing 100% oxygen on altitude decompression sickness

INTRODUCTION: Space Shuttle extravehicular activity (EVA) requires decompression from sea level pressure (14.7 psia) to a 4.3 psia (30,300 ft) pressure suit. The transition currently involves altering the shuttle atmosphere to allow shirt-sleeve denitrogenation to occur during a 12 to 36-h staged decompression (SD) at 10.2 psia (9,800 ft) with an oxygen-enriched breathing gas (26.5% oxygen, 73.5% nitrogen). The denitrogenation provides protection from decompression sickness (DCS) during EVA in a 4.3 psia pressure suit. Our goal was to determine the highest altitude at which SD while breathing 100% oxygen (SD100) could provide effective protection from development of DCS symptoms after further decompression to 29,500 ft (4.5 psia). METHODS: There were 30 male subjects exposed to at least 6 of 11 conditions in random order on successive months to 29,500 ft for 4 h while performing mild exercise and being monitored for venous gas emboli (VGE) with an echo-imaging system. The subjects received 15 min of ground-level (GL) preoxygenation and an additional 60 or 120 min of SD100 at one of four altitudes between 8,000 ft (10.9 psia) and 18,000 ft (7.3 psia). Control exposures followed a 75- or 135-min ground-level preoxygenation. RESULTS: During SD100, one case of DCS occurred at 18,000 ft, but not at lower staging altitudes. Higher levels of VGE were observed during SD100 at 18,000 ft than during SD100 at any lower altitude. CONCLUSION: Staged decompression at 16,000 ft and below results in decompression risk during subsequent decompression to 29,500 ft similar to that following equivalent periods of ground-level preoxygenation.     

呼吸不同浓度氧气对兔高空暴露的防护作用

目的 观察兔暴露于高空时呼吸不同浓度氧气后的生理变化和组织超微结构改变,探讨分子筛氧源在高空的防护效果。方法 将20只兔随机分为呼吸空气组(A)、呼吸63％富氧气体组(B)、呼吸83％富氧气体组(C)和呼吸纯氧组(D)。各组兔在低压舱内上升到11000m,停留30min,记录心脏区气泡、心电图和客观反应,观察心和脑组织超微结构的变化,肾组织促红细胞生成素(EPO)的表达。结果 空气组心脏区气泡数量明显增加,多数兔出现心律失常;富氧浓度组和纯氧组偶见气泡;随着吸人气氧浓度的增加,脑、心组织超微结构缺氧改变减轻,肾EPOmRNA表达的阳性率降低。结论 呼吸含氧浓度大于80％的富氧气体对高空暴露的机体有明显的防护作用。     

Exercise ending 30 min pre-dive has no effect on bubble formation in the rat

INTRODUCTION: We have previously shown that exercise performed 20 h before a dive significantly reduces bubble formation in both rats and humans. Furthermore, exercise performed closer to the dive did not prevent bubble formation. HYPOTHESIS: The present study was designed to determine whether exercise 30 min prior to a dive promotes bubble formation. The occurrence of many bubbles is linked to a higher risk of developing decompression sickness. METHODS: A total of 58 Sprague-Dawley rats were randomly divided into a sedentary control group (n = 29) and an exercise group (n = 29). Rats in the exercise group ran on a treadmill for a total of 90 min at variable intensity up to 85-90% of VO2max. Then, 30 min after exercise, one rat from each group rested in a pressure chamber at 700 kPa (7 atm) breathing air, performing a simulated dive. Bottom time was 45 min; decompression rate was 50 kPa x min(-1) (0.5 atm x min(-1)). Immediately after surfacing (100 kPa, 1 atm), the rats were anesthetized and bubbles were measured discontinuously for the next 60 min. RESULTS: There were no significant differences in survival (p = 0.55), median bubble grade (p = 0.67), survival time (p = 0.53), or the number of rats getting a bubble score > or = 2 (p = 0.79) between the groups. CONCLUSION: The same type and intensity of exercise that reduces bubble formation when performed 20 h prior to a dive neither promotes nor reduces bubble formation if performed 30 min before a dive. The present data indicate that exercise completed 30 min before a dive does not increase the risk of developing decompression sickness in the rat.     

Intracardial gas bubbles of altitude after negative pressure breathing.

The influence of negative pressure breathing on the appearance of intracardial gas bubbles at a subsequent decompression to altitude was investigated in five subjects using the precordial Doppler ultrasound technique. Every subject was tested for a suitable exposition that, after 30 min oxygen breathing at surface, caused both intracardial bubbles and decompression sickness. An identical exposition followed a week later, except that oxygen breathing at the surface now included negative pressure breathing. In all cases, negative pressure breathing caused a delay of the onset of both intracardial bubbles and bends and, in some cases, neither bubbles nor bends appeared at all. The total amount of bubbles was always less after negative pressure breathing. Thus, negative pressure breathing in connection with decompression may reduce the amount of intracardial bubbles and the risk of decompression sickness. This may be of importance in diving procedures and in the construction of diving devices.     

Exogenous nitric oxide and bubble formation in divers

PURPOSE: Prevention of bubble formation is a central goal in standard decompression procedures. Previously we have shown that exercise 20-24 h prior to a dive reduces bubble formation and increases survival in rats exposed to a simulated dive. Furthermore, we have demonstrated that nitric oxide (NO) may be involved in this protection; blocking the production of NO increases bubble formation while giving rats a long-lasting NO donor 20 h and immediately prior to a dive reduces bubble formation. This study determined whether a short-lasting NO donor, nitroglycerine, reduced bubble formation after standard dives and decompression in man. METHODS: A total of 16 experienced divers were randomly assigned into two groups. One group performed two dives to 30 m of seawater (msw) for 30 min breathing air, and performed exercise at an intensity corresponding to 30% of maximal oxygen uptake during the bottom time. The second group performed two simulated dives to 18 msw for 80 min breathing air in a hyperbaric chamber, and remained sedentary during the bottom period. The first dive for each diver served as the control dive, whereas the divers received 0.4 mg of nitroglycerine by oral spray 30 min before the second dive. Following the dive, gas bubbles in the pulmonary artery were recorded using ultrasound. RESULTS: The open-water dive resulted in significantly more gas bubbles than the dry dive (0.87 +/- 1.3 vs 0.12 +/- 0.23 bubbles per square centimeter). Nitroglycerine reduced bubble formation significantly in both dives from 0.87 +/- 1.3 to 0.32 +/- 0.7 in the in-water dive and from 0.12 +/- 0.23 to 0.03 +/- 0.03 bubbles per square centimeter in the chamber dive. CONCLUSION: The present study demonstrates that intake of a short-lasting NO donor reduces bubble formation following decompression after different dives.     

乙醇治疗急性减压病的实验研究

目的 探讨乙醇治疗急性减压病的病因学及其作用机制.方法 将实验兔32只复制成急性减压病(ADCS)模型,随机分为治疗组和对照组,每组16只.放人动物舱内在5 min内加压至0.6MPa,停留30 min,然后用10 min匀速减至常压(0.1 Mpa)出舱.出舱后每隔5 min定时测定Doppler气泡音.戊巴比妥纳20 mg/kg耳缘静脉麻醉后,手术暴露后腔静脉约10 cm作为观察段.治疗组ADCS模型兔在测定Doppler气泡音后,用25%乙醇溶液3 ml/kg,由耳缘静脉缓慢注射入血管内;对照组则由耳缘静脉缓慢注射10 ml生理盐水.然后经后腔静脉直接观察气泡消长情况,分次解剖,整体观察.结果 对照组16只兔,出舱后30 min相继死亡8只,其余在60～100 min时仍有Ⅰ～Ⅲ级Doppler气泡音,后腔静脉、皮下、肌肉、内脏器官及循环系统可见大量气泡,部分血管完全被气泡阻塞.治疗组无死亡,Doppler气泡音在30～60 min内消失.后腔静脉、皮下、肌肉、内脏器官的血管直径增加一倍以上,血流显著增快.血循环内无气泡或有极少量单个气泡.结论 乙醇疗法是一种快速有效、经济实用的消除急性减压病的新方法.     

Tissue nitrogen elimination in oxygen-breathing pigs is enhanced by fluorocarbon-derived intravascular micro-bubbles.

The present study tested the hypothesis that intravascular micro bubbles generated by i.v. infusion of a 2 % dodecafluoropentane (DDFP) emulsion will enhance tissue denitrogenation during oxygen breathing. Eleven spontaneously breathing pentobarbital anesthetized pigs were studied. Six pigs were treated with 0.08 ml/kg of DDFP-emulsion infused over 30 min and five (control) pigs received a matching dose of emulsion vehicle. Circulatory parameters were recorded. The pigs were connected via a tracheal tube to a closed circuit oxygen-primed breathing loop allowing volume measurements and nitrogen analysis by gas chromatography every 7 min. The nitrogen washout was recorded for up to four hrs in each group. The cumulative nitrogen yield during oxygen breathing was considerably larger in treated animals than in controls. Thus, the amount of nitrogen eliminated in the controls in 120 min was achieved already after 65 min in animals treated with the DDFP-emulsion. Blood pressure and cardiac output remained stable and were not different between the two groups during the four hrs of nitrogen washout. The central venous oxygen tension was significantly higher in the treated animals during oxygen breathing than in the controls. This difference was, in all probability due to enhanced oxygen transport by the micro-bubbles. CONCLUSION: Intravascular micro-bubbles generated by i.v. infusion of a small dose of 2 % DDFP-emulsion very effectively enhanced denitrogenation by oxygen breathing and deserve study as a means to improve prevention and treatment of decompression sickness.     

Exercise during a 3-min decompression stop reduces postdive venous gas bubbles

PURPOSE: Decompression sickness is initiated by the formation of gas bubbles in tissue and blood if the divers return to surface pressure too fast. The effect of exercise before, during, and after dive on bubble formation is still controversial. We have reported recently that strenuous aerobic exercise 24 h before simulated dive ameliorates venous bubble formation. The objective of this field study was to evaluate whether mild, continuous exercise during decompression has a similar impact. METHODS: Ten healthy, military male divers performed an open-sea field dive to 30 m of sea water breathing air, remaining at pressure for 30 min. During the bottom and decompression the subjects performed fin underwater swimming at about 30% of maximal oxygen uptake. Each diver underwent two randomly assigned dives, one with and one without exercise during the 3-min decompression period. Monitoring of venous gas emboli was performed in the right heart with ultrasonic scanner every 20 min for 60 min after reaching surface pressure in supine rest and during forced two-cough procedure. RESULTS: The study demonstrates that a mild, continuous exercise during decompression significantly reduced the average number of bubbles in the pulmonary artery from 0.9 +/- 0.8 to 0.3 +/- 0.5 bubbles per square centimeter in supine rest, as well as during two-cough procedure, which decreased from 4.6 +/- 4.5 to 0.9 +/- 0.9 bubbles per square centimeter. No symptoms of decompression sickness were observed in any subject. CONCLUSION: These results, obtained in the field conditions, indicate that a mild, underwater swimming during a 3-min decompression period reduces postdive gas bubbles formation.     

被动吸烟对豚鼠高空减压气泡生成影响的初步观察

观察了３０只豚鼠于密闭舱内被动吸入卷烟烟雾对随后高空减压心前区气泡出现的影响。结果表明：在上述２种吸入卷烟烟雾的条件下，减压气泡的首次出现时间和气泡等级与对照组相比无显著差异。初步提示减压露前短时间大量吸烟不会影响高空减压病的发生。