当归对宫内缺氧新生大鼠神经干细胞增殖、分化的影响

背景：实验小组前期研究发现孕鼠宫内缺氧可刺激胎鼠神经干细胞的增殖,缺氧6 h时增殖达高峰,在9 h也表现增殖,但能力开始下降。而缺氧达12 h时即表现为坏死或凋亡,但随缺氧天数的延长及时段的不同,对神经干细胞的影响又如何？ 目的：进一步探讨宫内缺氧对新生大鼠神经干细胞增殖、分化的影响及当归注射液的保护作用。 方法：孕 SD大鼠随机分为对照组、缺氧组和当归治疗组。孕14 d开始将当归组与缺氧组孕鼠置于三气培养箱中,制作缺氧性脑损伤新生鼠模型,此前1 h分别给于当归注射液和生理盐水尾静脉注射,对照组不缺氧,余同缺氧组。孕鼠分娩后立即取新生鼠大脑组织,经胶质纤维酸性蛋白、神经元特异性烯醇化酶免疫组织化学染色后行图像分析。 结果与结论：①缺氧组新生鼠海马胶质纤维酸性蛋白免疫组织化学阳性细胞的表达较相应对照组增加;而神经元特异性烯醇化酶免疫组织化学阳性细胞的表达较对照组减小。②当归治疗组新生鼠海马胶质纤维酸性蛋白免疫组织化学阳性细胞的表达较相应缺氧组减少;而神经元特异性烯醇化酶免疫组织化学阳性细胞的表达较对照组增大。结果表明,一定程度的缺氧可刺激神经干细胞增殖,并可刺激神经干细胞向神经胶质细胞分化,以及导致神经元的减少;当归注射液可减弱由于缺氧导致的神经干细胞的增殖和向胶质细胞分化的能力,并可缓解神经元的减少,提示当归可能对缺氧大鼠神经系统有一定的保护作用。     

激光调控内源性神经干细胞的增殖与分化

背景：大量研究表明增强脑内源性神经细胞的自我修复和增殖能力将成为治愈缺血缺氧性脑损伤最有价值的方法之一。 目的：探讨氦氖激光对新生大鼠缺血缺氧性脑损伤内源性神经干细胞增殖及分化的影响。 设计、时间及地点：随机对照动物实验,于2007-12/2008-05在郑州大学护理学院完成。 材料：7 d龄健康Wistar新生大鼠36只,随机分为假手术组、模型组、激光治疗组,12只/组。氦氖激光多功能治疗仪由桂林电子仪器厂生产。 方法：模型组、激光治疗组新生大鼠通过结扎左颈总动脉后,再吸入低浓度氧(含体积分数为8%的O2、体积分数为92%的N2)建立缺血缺氧性脑损伤模型;假手术组不结扎左颈总动脉,置于正常空气中。造模后第2天开始,激光治疗组给予氦氖激光照射,激光波长632.8 nm,激光功率4 mW,光斑直径3 mm,功率密度56.62 mV,能量密度33.975 J/cm2,10 min/次,1次/d,10 d为1个疗程,共2个疗程,两疗程间隔2 d。穴位选取顶骨正中的“百会”穴,以及第7颈椎与第1胸椎间、背部正中的“大椎”穴。疗程结束后制备脑海马切片,分别进行巢蛋白和微管关联蛋白2免疫组织化学染色。 主要观察指标：大鼠脑内巢蛋白标记的神经干细胞和微管关联蛋白2标记的神经元的表达情况。 结果：36只大鼠全部进入结果分析。①大鼠内源性神经干细胞的表达：与假手术组比较,模型组、激光治疗组齿状回内巢蛋白免疫阳性细胞均明显增多(F=122.36,P < 0.05),且激光治疗组增多幅度大于模型组(P < 0.05)。②神经元特有结构蛋白的表达：激光治疗组大脑皮质微管关联蛋白2表达相当广泛,强阳性染成棕褐色的树突呈条索样、流星样放射状分布,海马各区锥体神经元和齿状回颗粒细胞层神经元排列比较整齐,树突连续阳性染色呈树枝状交叉分布于分子层。假手术组与激光治疗组染色所见无明显差别。模型组微管关联蛋白2表达明显减弱。 结论：激光治疗能够促进缺血缺氧性脑损伤新生大鼠脑内源性神经干细胞增殖,并诱导其向神经元方向分化。     

脑源性神经营养因子促进bHLH基因的表达和神经干细胞的定向分化

目的观察脑源性神经营养因子(BDNF)对bHLH基因表达和神经干细胞(NSCs)定向分化的影响,探索NSCs分化的机制。方法取孕14 d的胚胎大鼠脑组织,以无血清培养基培养获得NSCs,然后随机分为2组,实验组加入5％胎牛血清(FBS)和20 ng/mL BDNF诱导其定向分化,而对照组仅加5％FBS,用免疫荧光及流式细胞仪的方法来检测分化得到的神经元细胞及其比例,采用RT-PCR技术分析bHLH基因表达的动态变化。结果实验组MAP-2阳性神经元的比例在分化培养后第3 d达高峰,约为60％,而同期对照组仅为30％,差异有统计学意义(P<0．05)。分化后bHLH基因MASH-1、neumD和neurogenin2表达均高于分化前,相同时间段实验组bHLH基因的表达强于对照组(P<0．05)。结论BDNF促进了NSCs向神经元定向分化;bHLH基因参与了NSCs的定向分化过程,其高表达可能有利于NSCs向神经元方向分化。     

脑源性神经营养因子对胎鼠神经干细胞向神经元方向分化的诱导

背景：神经元是中枢神经系统起主导功能的细胞，培养干细胞的最终目的是获得相应表型的神经元，从而促进中枢神经系统损伤的修复。但以往相关文献显示神经干细胞分化为神经元的比例不到30%。 目的：以脑源性神经营养因子作为诱导分化剂，观察其对胎鼠源性神经干细胞向神经元方向分化的作用。 设计、时间及地点：细胞学体外观察，于2006-06/2007-08在南京医科大学第一附属医院中心实验室完成。 材料：清洁级孕14~17 d的SD大鼠10只，诱导分化剂脑源性神经营养因子为Peprotech产品，胎牛血清为杭州四季青产品。 方法：孕鼠处死后取出胚胎，剪碎后机械法体外分离培养神经干细胞，锥虫蓝染色计数，调整细胞密度为2×106，添加B27及碱性成纤维细胞生长因子，置于37 ℃、体积分数为0.05的CO2恒温箱中原代培养，待细胞克隆球明显增大、中央变暗时传代扩增。将培养所得的干细胞克隆球分为2组，诱导组添加体积分数为0.01的胎牛血清+20 μg/L脑源性神经营养因子共培养，血清对照组仅添加体积分数为0.01的胎牛血清。 主要观察指标：在倒置显微镜下观察细胞生长、贴壁和分化情况。诱导分化5 d后，行神经元免疫组化鉴定，流式细胞仪检测神经元阳性细胞率。取原代培养未分化的神经干细胞及诱导分化3 d的两组细胞，RT-PCR检测内源性bHLH基因MASH-1的表达。 结果：原代培养可获得数十至数百个神经干细胞聚集在一起的神经克隆球，形态规则，立体感强；悬浮生长的克隆球经诱导分化后，逐渐失去其球状的立体外观，邻近克隆球发出的突起可相互连接，3 d后即有神经元、星形胶质细胞和少突胶质细胞从克隆周围出现。培养的神经干细胞呈巢蛋白阳性表达，诱导分化后呈微管相关蛋白2阳性表达。与血清对照组比较，诱导组神经元阳性细胞率显著升高（χ2=16.0，P < 0.05）。与未分化的神经干细胞比较，诱导组、血清对照组细胞MASH-1的表达均明显升高，且前者升高幅度明显强于后者（F=21.7，P < 0.05）。 结论：脑源性神经营养因子能促进神经干细胞向神经元方向分化，可能与内源性bHLH基因MASH-1的表达升高有关。     

肝细胞生长因子对神经干细胞分化的影响

目的体外培养获得神经干细胞并初步研究重组人肝细胞生长因子(human recombinant hepatocyte growth factor,HGF)对神经干细胞(neutal steal cells,NSCs)分化能力的影响。方法从胚胎大鼠脑组织中分离得到神经干细胞,并行免疫荧光鉴定。检测不同浓度的HGF(5ng/ml、10ng/ml、20ng/ml、40ng/ml)对神经干细胞分化的影响。结果体外培养的神经干细胞球巢蛋白(nestin)表达阳性,由神经干细胞球分化的细胞神经元特异性烯醇化酶(neuron specific enolase,NSE)和胶质纤维酸性蛋白(galial fibrillary acidic protein,GFAP)表达阳性。并且不同浓度HGF作用下的神经元细胞分化率不同。结论HGF对NSCs分化及较长时间存活具有重要作用,20ng/ml的HGF可以促进较好的分化效果。     

人神经干细胞移植到缺氧缺血性脑损伤新生大鼠脑内的存活及分布★

目的：新生儿缺氧缺血性脑病是导致脑性瘫痪的重要原因，至今缺乏有效疗法。将体外培养的人神经干细胞经脑室移植入缺氧缺血性脑损伤新生鼠，观察植入细胞在宿主脑内的存活、迁移及分化。 方法：实验于2005-01/09在解放军海军总医院儿科实验室完成。①对象：神经干细胞来源于孕12周流产的人胎儿脑组织，孕妇签署知情同意书，符合医院伦理委员会规定。清洁级SD新生鼠80只，随机数字表法分为细胞移植组、模型对照组，40只/组，实验过程中对动物的处置符合动物伦理学标准。②实验方法：取人胚胎脑组织，机械分散法分离单个核细胞，接种于添加表皮生长因子、碱性成纤维细胞生长因子、白血病抑制因子的N2培养基中，获取生长旺盛的人神经干细胞球，制成单细胞悬液，浓度约为5.0×1011 L-1，培养6 d后行PKH标记用于植入后示踪。两组新生鼠均建立缺氧缺血性脑损伤模型，造模后3 d，细胞移植组损伤侧脑室缓慢注入5 μL人神经干细胞悬液，模型对照组于相同部位注入等量生理盐水。③实验评估：取未经PKH标记的细胞球， 通过免疫细胞化学染色鉴定巢蛋白的表达及其向神经元、星形胶质细胞的分化情况。分别于细胞移植后1，2，4周及3个月，常规取脑组织，行免疫组织化学和荧光分析，观察植入后细胞存活及分布情况。 结果：在造模及细胞移植过程中，因麻醉、出血细胞移植组新生鼠死亡5只，模型对照组死亡7只，存活率85%~90%。①神经干细胞的鉴定及分化：80％活细胞巢蛋白呈阳性表达，并可分化为神经元、星形胶质细胞。②神经干细胞植入后存活及分布情况：植入后1周，神经丝蛋白阳性细胞多位于损伤侧皮质及海马处，纹状体、脑干、小脑、嗅球也有少量分布。植入后2周，海马和皮质可见神经丝蛋白阳性细胞，胞体伸出的神经微丝更长，细胞数量与1周时基本相似。植入后4周及3个月时PKH阳性细胞数量明显减少。 结论：在含有表皮生长因子、碱性成纤维细胞生长因子、白血病抑制因子的N2培养基中形成的人神经干细胞球，具有良好的增殖能力，可分化为神经元，移植至缺血缺氧新生鼠脑中能够向损伤区迁移，分布范围广。     

葡萄糖浓度对原代培养神经干细胞增殖、分化的影响

目的探讨不同浓度葡萄糖对神经干细胞增殖、分化的影响。方法胚胎小鼠脑细胞原代培养并鉴定。生理浓度和高浓度葡萄糖培养及诱导分化后．四唑盐比色（MTT）法及免疫荧光法观察两组不同葡萄糖浓度对神经干细胞增殖、分化的影响。结果原代培养的神经球表达巢蛋白（hestin），神经球分化的细胞表达神经丝200（NF200）和胶质纤维酸性蛋白（GFAP）。与生理浓度葡萄糖相比，高浓度葡萄糖降低了神经干细胞的增殖活力：分化3d后，高糖组的NF200阳性细胞和GFAP阳性细胞比例高于生理浓度组（P〈0．01），而nestin阳性细胞比例则反之（P〈0．01）；分化10d后，神经干细胞完全分化，免疫荧光检测发现生理浓度葡萄糖提高了NF200阳性细胞比例。结论高糖损害了神经干细胞的增殖活性。加速了神经干细胞的早期分化．降低了神经元的分化率。     

星形胶质细胞源性因子对神经干细胞分化的实验研究

目的探讨星形胶质细胞源性因子对神经干细胞分化的影响。方法分离和培养新生大鼠脑组织的神经干细胞;采用差速贴壁法和振荡法分离纯化星形胶质细胞,用免疫细胞化学染色法,胶质纤维酸性蛋白(GFAP)标记星形胶质细胞,进行细胞的纯度鉴定;将星形胶质细胞和神经干细胞在互不接触的情况下进行共培养,免疫荧光法观察神经干细胞分化后神经元特异性烯醇化酶(NSE)、GFAP和酪氨酸羟化酶(TH)的表达。结果纯化的星形胶质细胞GFAP抗体标记阳性,细胞纯度达98%;星形胶质细胞与神经干细胞共培养时,神经干细胞贴壁分化加快,NSE阳性细胞及TH阳性细胞明显多于对照组(P<0·05)。结论星形胶质细胞源性因子可快速诱导神经干细胞向神经元细胞、包括多巴胺神经元细胞分化,提示星形胶质细胞支持神经元发生。     

去分化肌肉干细胞神经增殖与分化能力的研究

目的研究和鉴定去分化肌肉干细胞是否具有神经增殖和分化能力。方法使用不同的条件性培养基,对去分化肌肉干细胞依次进行神经增殖和神经分化诱导,并通过形态学、免疫细胞荧光化学、反转录聚合酶链式反应(RT-PCR)等手段加以鉴定。结果①去分化肌肉干细胞在神经增殖培养基诱导下,形成典型神经球(neurospheres)结构,5-乙炔基-2’脱氧尿嘧啶核苷(EdU)标记阳性,抗巢蛋白(Nestin)阳性;RT-PCR提示肌形成蛋白(myogenin)表达水平下调,而Nestin、干细胞抗原-1(Sca-1)表达上调。②经神经分化培养基诱导,神经球细胞可分化为形态学上典型的、抗中间神经丝蛋白(NFm)阳性神经元。结论去分化肌肉干细胞具有神经增殖和分化潜能。     

激光调控内源性神经干细胞的增殖分化及脑功能重建**☆

背景: 大量研究表明增强脑内源性神经细胞的增殖能力和自我修复将成为治愈缺血缺氧性脑损伤有价值的方法之一。 目的：观察氦氖激光对新生大鼠缺血缺氧性脑损伤内源性神经干细胞增殖分化及脑功能重建的影响。 方法：7 d龄健康Wistar新生大鼠,建立缺血缺氧性脑损伤模型后第2天开始,激光穴位照射组给予氦氖激光照射。穴位选取顶骨正中的“百会”穴,以及第7颈椎与第1胸椎间、背部正中的“大椎”穴。假手术组和模型组不给予激光照射。于第2疗程结束后,用Y-型迷宫检测各组大鼠的学习记忆能力。随后制备脑海马切片,分别进行巢蛋白和微管关联蛋白2免疫组织化学染色。 结果与结论：①激光穴位照射组大鼠的学习和记忆能力明显高于模型组(P < 0.05),但与假手术组相比,无明显差异(P > 0.05)。②大鼠内源性神经干细胞的表达：与假手术组比较,模型组、激光治疗组齿状回内巢蛋白免疫阳性细胞均明显增多(P < 0.05),且激光治疗组增多幅度大于模型组(P < 0.05)。③神经元特有结构蛋白的表达：激光治疗组大脑皮质微管关联蛋白2表达相当广泛,强阳性染成棕褐色的树突呈条索样、流星样放射状分布,海马各区锥体神经元和齿状回颗粒细胞层神经元排列比较整齐,树突连续阳性染色呈树枝状交叉分布于分子层。假手术组与激光治疗组染色所见无明显差别。模型组微管关联蛋白2表达明显减弱。结果提示激光治疗能够促进缺血缺氧性脑损伤新生大鼠脑内源性神经干细胞增殖,诱导其向神经元方向分化,并达到学习记忆功能的重建。     

Influence of hyperbaric oxygen on the differentiation of hypoxic/ischemic brain-derived neural stem cells

BACKGROUND: It has been previously shown that hyperbaric oxygen may promote proliferation of neural stem cells and reduce death of endogenous neural stem cells (NSCs).OBJECTIVE: To explore the effects of hyperbaric oxygen on the differentiation of hypoxic/ischemic brain-derived NSCs into neuron-like cells and compare with high-concentration oxygen and high pressure.DESIGN, TIME AND SETTING: An in vitro contrast study, performed at Laboratory of Neurology,Central South University between January and May 2006.MATERIALS: A hyperbaric oxygen chamber (YLC 0.5/1A) was provided by Wuhan Shipping Design Research Institute; mouse anti-rat microtubute-associated protein 2 monoclonal antibody by Jingmei Company, Beijing; mouse anti-rat glial fibrillary acidic protein monoclonal antibody by Neo Markers,USA; mouse anti-rat galactocerebroside monoclonal antibody by Santa Cruz Biotechnology Inc.,USA; and goat anti-mouse fluorescein isothiocyanate-labeled secondary antibody by Wuhan Boster Bioengineering Co., Ltd., China.METHODS: Brain-derived NSCs isolated from brain tissues of neonatal Sprague Dawiey rats werecloned and passaged, and assigned into five groups: normal control, model, high-concentration oxygen, high pressure, and hyperbaric oxygen groups. Cells in the four groups, excluding the normal control group, were incubated in serum-containing DMEM/F12 culture medium. Hypoxic/ischemic models of NSCs were established in an incubator comprising 93% N2, 5% CO2, and 2% O2.Thereafter, cells were continuously cultured as follows: compressed air (0.2 MPa, 1 hour, once a day)in the high pressure group, compressed air+a minimum of 80% O2 in the hyperbaric oxygen group,and a minimum of 80% O2 in the high-concentration oxygen group. Cells in the normal control and model groups were cultured as normal.MAIN OUTCOME MEASURES: At day 7 after culture, glial fibrillary acidic protein,microtubule-associated protein 2, and galactocerebroside immunofluorescence staining were examined to observe differentiation and calculate the percentage of NSCs differentiating into neuron-like cells or neuroglia-like cells.RESULTS: Neuron-like cells or neuroglia-like cells were visualized in all five groups. There were no significant differences in the percentage of differentiating cells between the hyperbaric oxygen group and the normal control group (P>0.05). The percentage of NSCs differentiating into neuron-like cells in the hyperbaric oxygen group was significantly greater than model, high-concentration oxygen, and high pressure groups; however, the percentage differentiating into neureglia-like cells was significantly lower (P<0.01).CONCLUSION: Hyperbaric oxygen promotes the differentiation of brain-derived neural stem cells into neuron-like cells but inhibits differentiation into neuroglia-like cells. Furthermore, the efficacy of hyperbaric oxygen is superior to high-concentration oxygen and high pressure.     

高压氧联合替莫唑胺对胶质瘤U251细胞的影响

目的研究高压氧(Hyperbaric Oxygen,HBO)联合替莫唑胺(Temozolomide)对人神经胶质瘤U251细胞株的的影响及其机制。方法实验分为4组:A组高压氧联合替莫唑胺组、B组高压氧组、C组替莫唑胺组、D组对照组。通过体外模拟缺氧微环境,用四甲基偶氮唑蓝法(MTT法)、碘化丙啶(PI)染色法、流式细胞仪分别检测细胞生长抑制率、细胞死亡率、细胞凋亡率。Elisa法检测缺氧诱导因子1-α(HIF1-α)和多药耐药相关蛋白-1(MRP-1)的表达情况。结果 1高压氧联合替莫唑胺组在细胞生长抑制率、细胞死亡率和细胞凋亡率上明显高于其他组,数值均有统计学意义(P<0.05)。2高压氧联合替莫唑胺组与高压氧组在HIF1-α和MRP-1上无统计学意义(P>0.05),与其他组有统计学意义(P<0.05)。结论高压氧够增强替莫唑胺化疗效果,高压氧纠正了肿瘤的缺氧环境,下调了HIF1-α和MRP-1的表达,这可能是治疗作用的关键所在。     

高压氧治疗可影响受损眼眶中视神经的三维有限元分析

实验选择右侧眼眶粉碎性骨折中年男性患者1例,根据其CT扫描的图像,建立带组织的眼部三维有限元模型,通过改变受损侧颅骨的弹性模量和外界压强,模拟分析视神经在高压氧环境下的受力情况。模拟结果显示,受损和完整眼眶侧的视神经最大应力值均发生在视神经和眼球的接触部位。当外界压强保持不变,随着受损眼眶侧的颅骨弹性模量的降低,受损眼眶侧的视神经应力逐渐增大,随着颅骨弹性模量的降低,视神经的应力显著增加,而完整侧的应力值变化不大。当颅骨弹性模量不变时,随着外界压强的增加,视神经的最大应力均迅速增加。说明在高压氧环境中,患者的视神经可能受到压迫,受损眼眶侧视神经的应力远远大于完整眼眶侧的视神经应力。     

Umbilical cord-derived mesenchymal stem cell transplantation combined with hyperbaric oxygen treatment for repair of traumatic brain injury

Transplantation of umbilical cord-derived mesenchymal stem cells(UC-MSCs) for repair of traumatic brain injury has been used in the clinic. Hyperbaric oxygen(HBO) treatment has long been widely used as an adjunctive therapy for treating traumatic brain injury. UC-MSC transplantation combined with HBO treatment is expected to yield better therapeutic effects on traumatic brain injury. In this study, we established rat models of severe traumatic brain injury by pressurized fluid(2.5–3.0 atm impact force). The injured rats were then administered UC-MSC transplantation via the tail vein in combination with HBO treatment. Compared with monotherapy, aquaporin 4 expression decreased in the injured rat brain, but growth-associated protein-43 expression, calaxon-like structures, and CM-Dil-positive cell number increased. Following combination therapy, however, rat cognitive and neurological function significantly improved. UC-MSC transplantation combined with HBO therapyfor repair of traumatic brain injury shows better therapeutic effects than monotherapy and significantly promotes recovery of neurological functions.     

早期高压氧治疗对急性脑梗死患者神经功能的影响

目的：探讨早期高压氧治疗对急性脑梗死患者的临床疗效及对神经功能的影响。方法118例ACI随机分为2组,均给予常规治疗,治疗组在常规治疗的基础上,在发病早期时（48 h内）,C T证实脑部无活动性出血,生命体征平稳,立即给予高压氧治疗。结果治疗组总有效率86.67％,对照组为63.79％,治疗组优于对照组,差异有统计学意义（ P＜0.05）;治疗后治疗组NIHSS评分较对照组低,差异有统计学意义（P＜0.05）;治疗组MBI评分较对照组低,差异有统计学意义（P＜0.05）。结论早期高压氧治疗ACI效果满意,且可显著改善患者的神经功能缺损,提高日常生活活动能力。     

Effect of hyperbaric oxygen on GABA transport in rat brain synaptosomes

Summary Initial velocities of uptake of GABA have been measured in rat brain synaptosomes from animals which had been exposed to oxygen at high pressure (OHP) and compared to similar measurements in normobaric controls. For hypothalamus, no changes in GABA uptake occurred subsequent to exposure to OHP. For cortical synaptosomes, however, exposure to OHP resulted in a decreased velocity of GABA uptake at all combinations of [Na] and [GABA] used. The OHP data were found to fit the same transport model as found previously for control data. Thus, OHP exposure did not alter the basic mechanism by which sodium and GABA interact with the carrier in the process of transport. However, the constants which quantitate the model were changed by OHP exposure. As a consequence, the several kinetic parameters which are calculated from the model change in the OHP animals. These kinetic parameters are compared to similar calculations for both normobaric control animals and normobaric aged animals. Although the effects of OHP do not precisely parallel the effects of aging, the alterations in kinetic parameters are in several ways similar in the aged and OHP animals.     

Repeated hyperbaric oxygen induces ischemic tolerance in gerbil hippocampus

Hyperbaric oxygen HBO; 100% oxygen at 2 atmospheres absolute was administered for 1 h to male Mongolian gerbils either for a single session or every other day for five sessions. Two days after HBO pretreatment, the gerbils were subjected to 5 min of forebrain ischemic by occlusion of both common carotid arteries under anesthesia. Seven days after recirculation, neuronal density per 1-mm length of the CAI sector in the hippocampus was significantly better preserved in the five-session HBO pretreatment group ( n = 10: 175.7 (47.8/mm, 54.9% of normal) than in the ischemic control group ( n = 10: 26.2 (11.6/mm, 8.0% of normal) and in the single-session HBO pretreatment group ( n = 7: 37.3 (21.7/mm, 11.4010 of normal). Immunohistochemical staining for the 72-kDa heat-shock protein (HSP-72) in the CAI sector performed 2 days following pretreatment revealed that the five-session HBO pretreatment increased the amount of HSP-72 present compared with that in the ischemic control group and in the single HBO pretreatment group. These results suggest that tolerance against ischemic neuronal damage was induced by repeated HBO pretreatment, which is thought to occur through the induction of HSP-72 synthesis.     

Aminooxyacetic acid provides transient protection against seizures induced by hyperbaric oxygen

In an attempt to demonstrate a protective effect against convulsions induced by hyperbaric oxygen (OHP), aminooxyacetic acid (AOAA at 2.5 mg/kg) was administered subcutaneously to 60 white leghorn cockerels (aged 21–28 days) at periods of 1–72 h before exposure to OHP. A transient protection was noted 1–8 h after administration of the AOAA. This took the form of a 51–67% increase in the latent period before OHP induced convulsions began. By 12 h after injection, the protective effect had disappeared. Thereafter a phase of increased susceptibility to hyperbaric oxygen commenced. This phase lasted for at least a further 60 h.     

Effect of hyperbaric oxygen treatment on immunological parameters in multiple sclerosis

Hyperbaric oxygen (HBO) treatment has been reported to cause amelioration of clinical symptoms in patients with multiple sclerosis (MS). We have treated 10 MS patients with hyperbaric oxygen (100% O2 at 2 atmospheres absolute for 90 min daily for a total of 20 exposures), and performed immunological studies on peripheral blood and cerebrospinal fluid (CSF). After treatment there was a significant increase in total and helper T lymphocyte counts in peripheral blood, as well as an increase in both E, Fc gamma and C3b receptor-bearing lymphocytes. The responses to the mitogens PHA, con A and PWM were unchanged. Granulocytes showed an increased proportion of Fc gamma receptor and C3b receptor positive cells after treatment. The O2 consumption of granulocytes also increased, but phagocytosis, as measured by chemiluminescence, was unchanged. Serum IgA levels were slightly increased, while IgG and IgM concentrations remained unchanged after treatment. Cerebrospinal fluid cell counts, protein and IgG concentrations, as well as IgG indexes remained unchanged.     

过度高压氧治疗对缺氧性脑病所致持续性植物状态预后的影响

目的研究过度高压氧治疗(HBO)对缺氧性脑病所致的持续性植物状态(PVS)患者预后的影响,探讨高压氧的治疗机制及过度治疗的不良影响。方法收集我院收治的缺氧性脑病致PVS患者60例,根据其高压氧治疗的病史分为常规HBO组,超长HBO组,未接受HBO治疗对照3组。以发病后6个月为观察点。观察指标包括PVS意识及预后评分(南京2001年版);改良Ashworth量表(MAS)评定;日抽搐次数;头CT/MRI中第三脑室宽度;颅内压;脑电图等。结果获得随访51例。3组患者在年龄、患病时间、意识及脑电图无显著性差异。第三脑室宽度及颅内压数据分析,超长HBO组的第三脑室宽度明显大于常规HBO组与对照组,同时颅内压较低,且这种差异在预后恢复有显著性差异(P0.05)。肌张力评定提示对照组及常规HBO组统计学分析无显著性差异。但与超长HBO组肌张力明显高于其他组,有显著性差异(P0.05)。超长组中抽搐次数较其他2组增加,但无统计学差异。结论高压氧治疗对脑损伤后意识恢复具有一定的疗效,但过度高压氧治疗可能导致脑昏迷患者严重的脑萎缩、巨大脑室及低颅压状态。形成不可逆、迟发性脑损伤,影响意识恢复。因此需合理、规范应用高压氧治疗。