高压氧反复暴露对小鼠脑内促红细胞生成素含量的影响

目的 通过对脑内促红细胞生成素（EPO）的检测，探讨高压氧（HBO）反复暴露增强低氧耐受能力是否与EPO有关。方法 昆明小鼠54只，随机分为3组：（1）HBO组：实验动物置密闭氧舱内供给医用纯氧，每天2次，每次60min，连续3d。供气压力第1—3天分别为150，200和250kPa（绝对压）；（2）高压空气（HPA）组：舱内供给常氧氮混合气，其他处理同HBO组；（3）空白对照（NC）组：仅在每天同一时间模拟进出舱活动，不作其它处理。处理结束后24h，①将每组10只动物同时置密闭氧舱内，进行低氧耐受实验。舱内持续供给5％O2-95％N2混合气体，压力为常压，记录每只动物在常压低氧状态下的生存时间；②同时将每组8只动物分别按实验要求取材，用免疫组化法检测各组动物脑内EPO阳性细胞表达情况。结果低氧生存时间测定结果表明，HBO组低氧生存时间较其它两组明显延长。免疫组化结果显示，与NC组相比，HPA组脑内各脑区EPO阳性细胞数均未发现明显改变；与HPA组相比，HBO反复暴露3d后，小鼠脑内EPO阳性细胞数发生明显改变，大脑皮层和海马EPO阳性细胞数显著增多。结论HBO反复暴露能增加小鼠低氧耐受能力；HBO反复暴露能增加小鼠脑内EPO含量，这可能是HB0反复暴露增强动物低氢耐罟能力的重要机制之一。     

高压氧对豚鼠庆大霉素中毒耳蜗微循环的影响

目的　探讨高压氧 (HBO)对药物中毒耳蜗微循环的影响。方法　实验组 54只豚鼠腹腔注射庆大霉素 1 50 m g· kg- 1 · d- 1 ,连续注射 5d,造成耳聋。第 6天将豚鼠随机分为耳聋 (A)组、耳聋 高压空气 (B)组 ,耳聋 HBO(C)组 ,每组 1 8只动物 ,再按不同暴露时间各分成 3个小组。B组和 C组分别给予高压空气和 HBO 0 .2 MPa暴露 ,每天 1次。正常对照组 6只豚鼠不作任何处理。于药物注射前及耳聋后 1 ,1 0 ,2 0 d分别以听觉脑干诱发电位 (ABR)仪检测耳蜗听功能 ,以激光多普勒血流仪 (L DF)检测耳蜗血流量 (CBF) ,处死动物后行耳蜗毛细胞扫描电镜观察。结果　实验组较对照组动物 ABR阈移及CBF均显著降低 (P<0 .0 1 ) ,毛细胞形态明显受损。其中 C组较 A和 B组的 CBF增高 ,差异有非常显著性 (P<0 .0 1 )。结论　 HBO可以显著提高豚鼠庆大霉素中毒耳蜗的血流量 ,改善了耳蜗的微循环 ,可能有助于药物聋的防治     

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.     

重复+Gz暴露后大鼠心室肌的形态学改变

目的探讨不同水平的持续1周的＋Gz重复暴露后大鼠心室肌形态学的改变。方法24只雄性SD大鼠随机分为对照组、＋6Gz组和＋10Gz组，每组8只。＋6Gz组和＋10Gz组大鼠分别暴露于＋6Gz／3min和＋10Gz／3min，1次／d，共1周；分别于末次暴露后即刻、1d取心室肌做苏木精-伊红（HE）染色和透射电镜观察。结果HE染色心室肌无明显变化。电镜下可见，＋6Gz重复暴露后心室肌肌丝排列基本整齐，肌浆网轻度扩张，细胞连接扩大，间质水肿，微血管扩张；＋10Gz重复暴露后心室肌细胞水肿，核内异染色质边集，肌浆网明显扩张，线粒体反应性增生，空泡化，闰盘连接完全破坏。重复暴露后1d较即刻心室肌超微结构变化更明显。结论＋6Gz／3min重复暴露1周可引起大鼠心室肌超微结构轻微改变，而＋10Gz／3min重复暴露1周可造成大鼠心室肌超微结构的明显改变。     

+Gz暴露后大鼠相关血管活性物质的变化

目的 探讨 Gz暴露后大鼠血浆一氧化氮(NO)、内皮素(ET-1)、肾上腺髓质素(ADM)的变化，为 Gz防护研究提供实验依据。方法 30只雄性Wistar大鼠随机分成对照组、 5Gz及 10Gz暴露后30min及6h五组，每组6只。分别于暴露后30min和6h后处死大鼠取血及心脏、肺组织，测定血浆NO、ET-1、ADM含量及反转录聚合酶链反应(RT-PCR)定量检测方法检测心脏、肺组织eNOSmRNA表达水平。结果 Gz暴露后大鼠血浆中NO、ADM含量及心脏和肺组织eNOSmRNA表达水平显著增高，血浆中ET-1含量显著减低。结论 Gz暴露后大鼠NO、ET-1、ADM出现抗损伤代偿性改变。     

+Gz重复暴露后兔颈椎间盘BMP表达和影像学改变

目的：探讨＋Gz重复暴露对兔颈椎影像学和椎间盘骨形态发生蛋白（BMP）表达的影响。方法：15只兔随机分为对照组、＋G2暴露1d组、2周组、4周组、6周组。每组3只。＋Gz暴露组兔每天连续5次暴露于＋6Gz、持续45s，中间间歇5min。各组动物均于实验前后颈椎侧位拍片作自身对比，实验结束后气栓法处死并取颈椎做BMP免疫组化分析。结果：X线片显示对照组、＋Gz暴露1d组及2周组兔颈椎无明显变化，而＋Gz暴露4周组和6周组兔颈椎均出现显著退行性改变。对照组、＋Gz暴露1d、2周和4周组兔颈椎间盘未见BMP阳性细胞表达，＋Gz暴露6周组兔颈椎间盘的纤维环中可见少量散在分布的BMP阳性表达的软骨细胞。结论：＋6Gz重复暴露4周和6周可引起兔颈椎发生退行性改变和椎间盘BMP的表达。     

高、低压舱致豚鼠耳气压损伤的形态学变化

目的 验证高压氧舱法和低压舱法检测咽鼓管通气功能时，引起实验豚鼠的中耳、内耳病理改变的一致性。方法 健康的杂色豚鼠38只随机分为3个高压氧舱组和3个低压舱组，分别在相应条件下进行模拟上升和下降实验，出舱电耳镜观察豚鼠鼓膜后处死，进行中耳及内耳组织学观察。结果 鼓膜反应及中耳、内耳组织学改变组间无差异。结论 本实验从病理形态学角度证实高压氧舱可以检测咽鼓管通气功能。     

Contractile function of the heart of guinea pigs after long-term continuous stress

Guinea-pigs exposed to 60- and 100-day biosocial stress were used to examine the contractile function of the heart in the whole body and in an isolated state. A 60-day stress effect caused adaptation which included increases in the intensity of heart contractility and in its weight unit by 29% and 38%, respectively. Measurement of resistance of such an adapted heart to isometric load produced by a short-term aortic occlusion showed increases in maximal rates of its contraction and relaxation by 34-35%. After a 100-day stress-effect the strength and velocity of heart contraction and resistance to isometric load returned to normal; however, the intensity of the function of the weight unit increased by 27-32%. The effect of adaptation was also seen in an isolated heart: after a 100-day exposure the isolated hearts did not lose their ability to react to a greater preload according to Starling's law; moreover at the filling pressure 15 cm H2O their cardiac output increased by 50% as compared to the baseline. This observation suggests that the process of adaptation of guinea-pig hearts to chronic stress involves not only activation of central mechanisms of regulation but also enhancement of mechanisms of self-regulation but also enhancement of mechanisms of self-regulation.     

不同+Gz重复暴露下大鼠不同脑区热休克蛋白-70的表达

目的 探讨不同 Gz重复暴露后,大鼠不同脑区热休克蛋白-70（HSP70)表达强度和时程的变化规律。及其与正加速度致脑损伤的相关性。方法 将雄性SD大鼠随机分为对照组、 2Gz、 6Gz和 10Gz暴露组。分别在暴露后6h、1d、2d、4d和6d处死取脑,利用HE和免疫组织化学染色,观察HSP70在鼠脑不同部位的表达。及脑神经元形态学和血脑屏障通透性的变化,结果 G2重复暴露可诱导HSP70的表达。其表达强度,持续时间和部位随G值而异。低G值（ 2Gz)下,表达强度弱,持续时间短,但范围较广;高G值（ 10Gz)下,表达仅局限在下丘脑和梨状皮层等部位。呈中等强度反应;中等强度G值（ 6Gz)下,表达范围广（在皮层、海马、丘脑等部位均有HSP70较强反应）,持续时间长。结论 6Gz诱导的HSP70表达最强,持续时间最长。为研究热休克蛋白对正加速度致脑损伤的保护作用。提供了实验依据。     

持续高加速度重复作用对大鼠颞下颌关节的影响

目的 观察持续性高正加速度重复作用对大鼠颞下颌关节的影响。方法 雄性Wis-tar大鼠40只随机分成4组：A组为空白对照：B组地面固定5min;C组固定于离心机转臂上,俯卧位,头向轴心, 1Gz离心5min;D组体位同C组, 10Gz离心30s,G增长率约0.5G/s,间隔时 1Gz离心60s,连续5次/d,每周4天,共3周,各组动物分别取颞下颌关节作光镜观察,扫描电镜和透射电镜观察。结果 A组、B组和C组未见异常,D组光镜观察;髁状突和关节盘胶原纤维排列紊乱、断裂,可见成纤维细胞变性和细胞核分裂象;扫描电镜观察;髁状突和关节盘凝胶状物质缺失,胶原纤维暴露断裂;透射电镜观察;髁状突和关节盘胶原纤维排列紊乱,成纤维细胞空泡变性。线粒体嵴变形或消失,软骨细胞粗面内质网发达。结论 高正加速度重复性暴露可导致大鼠颞下颌关节的损伤。     

Oxidative metabolism in platelets, platelet aggregation, and hematology in patients undergoing multiple hyperbaric oxygen exposures.

Repeated hyperbaric oxygen (HBO2) treatments at 2.2 ATA for 90 minutes each are used to treat chronically ill patients with problem wounds, but there are concerns about the cytotoxicity of oxygen to blood cells and platelet function during prolonged HBO2 therapy. We recruited 31 consenting patients scheduled for multiple HBO2 treatments to evaluate oxidative metabolism in platelets, platelet aggregation, and hematology (mean age +/- standard error, 61 +/- 2.6 years, 20 males, 11 females). Venous blood was collected before and after the 1st and 20th HBO2 treatments. No effect of HBO2 was observed on red cell counts, hematocrit, hemoglobin, mean red cell volume (MCV), platelet counts, basal levels of lactate production by platelets, ferric reducing ability of plasma (FRAP), or plasma protein. The capacity for oxidative metabolism (lactate ratio) in platelets was not affected by HBO2, except in smokers where it increased by the 20th HBO2 treatment. Mean lymphocyte count was increased by 38% after the 20th treatment. There was also a 23% increase in platelet protein content, and a 24% increase in arachidonic acid-dependent platelet activation. Collagen-dependent platelet aggregation was unaffected. Blood glucose showed HBO2-dependent variability, but remained in the normal range. Plasma lactate levels decreased significantly from 3.2 to 2.5 mmol/l by the end of the study. Overall, we found no evidence that 20 HBO2 sessions caused adverse effects on platelet aggregation or oxidative metabolism in platelets, red or white cell counts, or total antioxidant status of the plasma.     

Venous gas embolism in chamber attendants after hyperbaric exposure.

An initial occupational survey (OS) was initiated to investigate the prevalence of venous gas embolism (VGE) in chamber attendants assisting hyperbaric oxygen (HBO2) treatments. Nine female subjects were exposed for three consecutive days to the routine hospital procedure of compressed air exposure to 240 kPa for approximately 115 min with 12 min of terminal oxygen (O2) breathing. VGE was monitored with ultrasound Doppler in 15 min intervals for 2h after the first and third exposure. A follow-up experimental study was completed to investigate whether changed breathing gases and decompression would affect the high incidence of VGE observed in the OS. Ten female subjects were randomly exposed to the routine or revised profile (12 and 24 min of terminal O2 breathing respectively), and a Nitrox profile (breathing gas 40.5% O2 in Nitrogen during 90 min of the isobaric phase). VGE was monitored with transthoracic ultrasound scanner and Doppler. In the OS precordial VGE grade III (Doppler) was observed in five subjects, but median resting precordial VGE was Grade 0 both days and VGE score at all sites were equal Days 1 and 3. In the experimental study, median resting precordial VGE was Grade 0 (Doppler) and Grade 1 (Scanner). VGE Grade III (Doppler) was observed in all series, but VGE scores were not significantly different between the series. We conclude that chamber attendants assisting HBO2 treatment at 240 kPa for approximately 115 min are exposed to a significant decompression stress using the profiles tested in the present study.     

Pulmonary effects of submerged oxygen breathing in resting divers: repeated exposures to 140 kPa.

To detect cumulative effects of and check required recovery times between underwater exposures to 130-140 kPa oxygen, we assessed pulmonary oxygen toxicity after resting dives for four and six hours on two, five, and six or ten days, and three hours twice on each of two days. Despite a slight downward trend in diffusing capacity, four-hour resting dives could be repeated for at least ten days if intervals between them were 20 hours: 17% of divers had mild symptoms; 5%, mild changes in flow-volume parameters. In contrast, six-hour resting dives caused symptoms in 33% of divers. When dives were repeated daily (after 18 hours), but not with one day off (after 42 hours), changes in diffusing capacity accumulated, and hyperoxic myopia occurred after five dives. Divers complained of fatigue more with daily than with alternate day dives. When daily exposure was split into two three-hour dives, the incidences of symptoms and changes in pulmonary function depended on the surface intervals: on the second day, with two and 16 hours between dives, two three-hour dives were similar to a six-hour dive; with four and 14 hours, to a four-hour dive; with six and 12 hours, to a six-hour dive.     

高持续性＋Gz重复暴露对大鼠血脑屏障通透性的影响

目的观察在离心机高Ｇ值反复作用下，血脑屏障通透性的变化特点，为高Ｇ值作用下脑功能改变的解释提供生理学依据。方法选雄性大鼠２０只，分为对照组及＋ＧＺ暴露后不同时间组，实验组经增长率为１Ｇ／ｓ，持续３ｍｉｎ的＋１０ＧＺ暴露３次，立即经大鼠心脏灌注镧固定液，开颅取脑，制成切片，置透射电镜下观察。结果＋ＧＺ重复暴露３次后即刻，即见镧颗粒通过少数开放的毛细血管内皮细胞间的紧密连接，沉积于血管外围；暴露后１ｈ及６ｈ，可见大部分毛细血管内皮细胞间的紧密连接开放，镧颗粒弥漫性地分布于神经细胞间隙，部分镧颗粒已进入神经细胞内部，分布于线粒体、内质网等细胞器的表面；暴露后２４ｈ，则见镧颗粒仅局限分布在血管腔内，毛细血管外的间隙则未见镧颗粒沉积，与对照组大鼠相似。结论＋１０ＧＺ／３ｍｉｎ重复作用３次可引起大鼠血脑屏障通透性增加，这种改变是可逆的。其可能在＋ＧＺ致脑水肿的发生、发展过程中起重要作用。     

中耳加压治疗豚鼠内淋巴积水

目的　探讨中耳加压治疗是否可抑制豚鼠内淋巴积水。方法　 4 2只豚鼠随机分为 4组 :对照组 10只 ,双耳未手术 ;32只豚鼠右耳制备内淋巴积水的动物模型 :积水 4周组 10只 ,积水 8周组 10只 ,加压组 12只。加压组豚鼠在术后第 5周起在压力舱内进行加压治疗 ,共 3周。观察 4组动物耳蜗形态和功能的变化。结果　加压组右耳 70 d B SPL - SP/ AP值、最大中阶面积 (SMA )比率 (分别 0 .2 9±0 .0 9,2 .2 3± 0 .2 0 )与相同生存期的积水 8周组 (分别为 0 .6 9± 0 .15 ,4 .0 1± 0 .5 2 )相比显著减小 (P<0 .0 5 ) ,而与积水 4周组 (分别为 0 .2 9± 0 .13,2 .2 2± 0 .2 0 )差异不显著 (P>0 .0 5 )。加压组右耳听觉脑干电反应 (ABR)听阈 [(36 .6 7± 14 .30 ) d B SPL ]低于积水 8周组 [(44 .0 0± 14 .30 ) d B SPL ],但差别无统计学意义 (P>0 .0 5 )。结论　加压治疗可显著抑制内淋巴积水的发展 ,并改善耳蜗功能。为梅尼埃病的治疗寻找一种无创伤性方法——加压治疗提供实验依据。