0.65 MPa氦氧暴露对潜水员记忆和空间推理能力的影响

目的 观察0.65 MPa氦氧环境下潜水员记忆和空间能力的变化及对潜水员心理的影响.方法 采用棋盘空间记忆广度和折纸空间推理的方法 ,分别对7名专业潜水员进行测量,比较他们在常压和0.65 MPa氦氧环境中的成绩.结果 7名被试者在常压和0.65 MPa氦氧环境中棋盘空间广度记忆测验结果 ,除1人外其他被试者测试成绩均发生了变化,暴露前后比较差异有统计学意义(P<0.05).空间推理能力测验结果 显示存在明显个体差异,0.65 MPa氦氧环境中的测试成绩普遍低于常压环境.结论 氦氧暴露后潜水员的记忆能力和空间推理能力有一定的下降,其发生的机制还需要进一步探讨.     

0.65 MPa氦氧暴露对潜水员记忆和空间推理能力的影响

目的 观察0.65 MPa氦氧环境下潜水员记忆和空间能力的变化及对潜水员心理的影响.方法 采用棋盘空间记忆广度和折纸空间推理的方法 ,分别对7名专业潜水员进行测量,比较他们在常压和0.65 MPa氦氧环境中的成绩.结果 7名被试者在常压和0.65 MPa氦氧环境中棋盘空间广度记忆测验结果 ,除1人外其他被试者测试成绩均发生了变化,暴露前后比较差异有统计学意义(P<0.05).空间推理能力测验结果 显示存在明显个体差异,0.65 MPa氦氧环境中的测试成绩普遍低于常压环境.结论 氦氧暴露后潜水员的记忆能力和空间推理能力有一定的下降,其发生的机制还需要进一步探讨.     

0.65 MPa氦氧暴露对潜水员记忆和空间推理能力的影响

目的 观察0.65 MPa氦氧环境下潜水员记忆和空间能力的变化及对潜水员心理的影响.方法 采用棋盘空间记忆广度和折纸空间推理的方法 ,分别对7名专业潜水员进行测量,比较他们在常压和0.65 MPa氦氧环境中的成绩.结果 7名被试者在常压和0.65 MPa氦氧环境中棋盘空间广度记忆测验结果 ,除1人外其他被试者测试成绩均发生了变化,暴露前后比较差异有统计学意义(P<0.05).空间推理能力测验结果 显示存在明显个体差异,0.65 MPa氦氧环境中的测试成绩普遍低于常压环境.结论 氦氧暴露后潜水员的记忆能力和空间推理能力有一定的下降,其发生的机制还需要进一步探讨.     

氢氧高压环境下小鼠脑电图功率谱和睡眠周期的变化

目的探讨高压氢氧环境对小鼠睡眠的影响。方法将小鼠暴露于2．1MPa．氢氧环境中10h，连续记录小鼠脑电图（EEG），进行EEG密度功率谱分析。结果在氢氧环境下，除了个别动物出现可逆的6段活动受抑制外，多数动物EEG密度谱中表示动物清醒和睡眠状态的密度疏密交替的特征始终存在。结论在2．1MPa氢氧环境下个别小鼠觉醒度提高，但总体上睡眠节律保持完好。同时，由于密度谱可以动态反映高压下动物EEG变化趋势和个体差异，提示用这一分析方法进行压力负荷监护的可能性。     

脑活素对大鼠及小鼠缺氧的保护作用

目的：观察脑活素对小鼠及大鼠胚脑组织细胞缺氧时的保护作用。方法：用ＴＢＡ微量法测量小鼠脑组织中过氧化脂质的含量;按邹氏法检测及观察培养大鼠胚鼠脑细胞存活状况,计算存活率。结果：脑活素组中小鼠脑组织匀浆过氧化脂质含量及胚鼠脑细胞存活率均较对照组有显著性差异（前者Ｐ＜ ０．０１;后者Ｐ＜ ０．０５） 。结论：脑活素具有明显的抑制自由基产生,提高脑组织细胞抗缺氧能力,从而具有保护脑细胞的作用。     

4.6 MPa氦-氧对小鼠脑细胞外液谷氨酸浓度的影响

目的阐明高气压对脑细胞外液谷氨酸浓度的影响。方法将清醒的７只小鼠在３０分钟内快速加压至４．６ＭＰａＨｅ－Ｏ２环境。采用微透析技术，通过预先植入海马部位的微透析探头收集脑细胞外液，然后用高效液相（ＨＰＬＣ）梯度洗脱分离，以荧光检测法分析氨基酸含量。高压暴露下全过程用连续脑电振幅谱方式监视动物大脑功能状态。结果发现小鼠脑细胞外液谷氨酸浓度在４．６ＭＰａＨｅ－Ｏ２环境下是升高的（透析液中浓度增加了０．２６μｍｏｌ／Ｌ，Ｐ＜０．０５）；脑电的主要变化有振波向低频转移，振幅减弱并阵发性增强及出现尖峰（ｓｐｉｋｅ）等。癫痫样脑电出现在脑细胞外液谷氨酸过度升高的动物。结论以上结果说明高气压下中枢神经系统功能随细胞外液谷氨酸浓度升高而扰乱，是导致高压神经综合征（ＨＰＮＳ）的重要原因。脑细胞外液谷氨酸浓度在高气压下变化的差异可能是ＨＰＮＳ个体差异的原因之一。     

高压氧预暴露对急性氧中毒大鼠模型惊厥潜伏期影响的实验研究

目的 研究高压氧预暴露对大鼠急性氧中毒潜伏期的影响并探讨其机制.方法 将40只Sprague-Dawley(SD)大鼠随机分为对照组和高压氧预暴露组,每组20只,其中高压氧预暴露组于高压纯氧(0.3 MPa)下暴露20 min,然后减至常压行空气通风20 min,如此循环4次.24 h后,将2组大鼠暴露于高压纯氧(0.5 MPa),观察40 min.检测指标包括惊厥潜伏期变化、大鼠脑组织中超氧化物歧化酶(SOD)活性和一氧化氮(NO)含量变化,进行HE染色以观察脑组织病理改变.结果 高压氧预暴露后,大鼠惊厥潜伏期[(29.79±2.13)min]比对照组[(24.25±3.76)min]延长,脑组织NO含量[(2.93±0.39)nmol/g]比对照组[(7.46±1.11)nmol/g]减少,而SOD活性与HE染色结果 显示2组差异无统计学意义.结论 高压氧预暴露可以延长大鼠惊厥潜伏期,其机制可能是高压氧降低了脑组织中的NO含量.     

NaHCO3对氧惊厥潜伏期的影响

目的观察NaHCO3对氧惊厥潜伏期的影响，以探讨内源性CO2与氧惊厥的关系。方法在复制小鼠氧惊厥模型的基础上，行为学方法测定不同压力下氧惊厥潜伏期。小鼠24只，随机分为6组：3、4、5ATA下，分别设生理盐水组、5％NaHCO3组，每组4只。另取小鼠15只，随机分为3组：常压对照组、生理盐水组和5％NaHCO3组，每组5只。后2组在4ATA医用纯氧下暴露18min后，测定脑组织氧化产物丙二醛（maleic dialdehyde，MDA）含量。结果（1）与生理盐水组相比，5ATA下，5％NaHCO3组的氧惊厥潜伏期明显延长（P〈0．01）；4ATA下，5％NaHCO3组的氧惊厥潜伏期也延长（P〈0．01）；3ATA下，由于120min后小鼠仍未发生惊厥，所以不能作出判定。（2）4ATA高压氧暴露18min后，5％NaHCO3组与生理盐水组的脑组织MDA含量明显低于常压对照组；5％NaHCO3组的脑组织MDA含量明显低于生理盐水组（P〈0．05）。结论5％NaHCO3可以延长氧惊厥潜伏期，减轻脑组织氧化损伤程度。     

快速减压对豚鼠脑组织中前列腺素的影响

目的：探讨快速减压对豚鼠脑组织中前列腺素的影响。方法：将豚鼠分为快速减压组和对照组，快速减压组动物置于小加压舱内，5min加压至0．6MPa,并在该压力下暴露60min，用19min减压至常压出舱；对照组不进行加减压处理。在实验结束时处死动物取脑皮质，用酶免测定法测定组织中前列腺素E2（PGE2），血栓素B2（TXB2）和6－酮－前列腺素F1a(6-K-PGF1a)含量。结果：快速减压后，脑后质中的PGF2为对照组的2倍，TXB2为对照组的3倍，6－K－PGF1a为对照组的2．6倍，3种PGs与对照组比均有非常显著性差异（P＜0．01）。结论：快速减压可引起机体脑组织中不同前列腺素含量明显升高，PGs在脑组织应激损伤中起重要作用。     

高压氧对大鼠局灶性脑缺血再灌注时神经元特异性烯醇化酶的影响

目的研究高压氧(HBO)对大鼠局灶性脑缺血再灌注(IR)时．大鼠脑梗塞体积．脑组织病理改变及神经元特异性烯醇化酶(NSE)含量的影响。方法用线栓法制备阻断大脑中动脉(MCA)的局灶性脑IR模型。Wistar大鼠30只，随机分为5组：正常对照组(N组n=-6)，缺血再灌注2h 常压空气组(Rt组,n=-6)，缺血再灌注24h 常压空气组(R2组，n=-6)，缺血再灌注2h HBO组(H1组，n=-6)，缺血再灌注24h HBO组(H2组，n=-6)。R1、R2、H1、H2组缺血时间均为2h。R1、R2组暴露于常压空气，H1、H2组暴露于2．5MPa氧气。病理切片用HE染色，用Swanson方法测定脑梗塞体积，用酶联免疫法测定NSE含量。结果H1、H2组与R1、R2组相比，神经元缺血性损害较轻，脑梗塞体积缩小，NSE含量明显下降，差异有统计学意义。结论HBO能减轻缺血性脑损害，保护脑组织。     

Effect of 2.1 MPa and 4.1 MPa H2O2 exposure on auditory brain stem evoked potential in mice.

Brain auditory evoked potential (BAEP) in mice exposed to hyperbaric H2O2 pressure was monitored to reveal the correlation between altered synaptic transmission and hydrogen narcosis or isobaric HPNS. Inter peak latencies and wave amplitudes were selected as indices of assessment. The animals were exposed either to He-O2 or H2-O2 at 2.1 MPa and 4.1 MPa. Results showed that synaptic transmission was inhibited to various extents. The inhibition was partly due to the narcotic effect of hydrogen, which was added to the effect caused by hydrostatic pressure. On the other hand, asymmetrical reaction of each segment in the neuro-network might be responsible for the occurrence of HPNS.     

Role of oxidative stress and inflammation in hypoxia-induced cerebral edema: a molecular approach

The present study reports the possible role of oxidative stress and inflammation (role of nuclear factor, NFkB) in hypoxia-induced transvascular leakage in brain of rats. The rats were exposed to a simulated altitude of 25,000 ft for different durations: 0, 3, 6, 12, 24, and 48h. Brain water content, transvascular leakage, oxidative stress, and proinflammatory parameters were studied at different durations of hypoxic exposure. The results revealed that maximum increase in transvascular leakage in brain of rats was observed at 24h of hypoxic exposure (240.16 ± 1.95 relative fluorescence units (r.f.u)/g tissue) compared with control (100.58 ± 1.79 r.f.u/g tissue). There was a significant increase in reactive oxygen species (ROS) and lipid peroxidation (MDA), with concomitant reduction in antioxidants. Hypoxic exposure resulted in a significant increase in NFκB protein expression levels and in the DNA binding activity in the 24-h hypoxic exposure (p<0.001) compared with control. There was a significant increase in proinflammatory cytokines, with concomitant upregulation of cell adhesion molecules. Simultaneously, to rule out the fact that inflammation causes cerebral edema, the rats were pretreated with curcumin (100 mg/kg body weight) 1h prior to 24-h hypoxia. Curcumin pretreatment significantly attenuated the hypoxia-induced cerebral transvascular leakage (p<0.05), with concomitant downregulation in the expression of brain NFκB levels (p<0.001). The present study therefore reveals that inflammation (NFκB) plays a significant role in hypoxia-induced cerebral edema.     

不同强度微波辐射对小鼠脑组织钙、镁ATP酶活性的影响

目的　探讨微波对机体中枢神经系统作用的机理。　方法　用 2 45 0 MHz连续波微波理疗机为辐射源 ,以昆明小鼠为对象 ,观察在 1m W/ cm2、5 m W/ cm2和 10 m W/ cm2三种照射强度下 ,小鼠脑皮层、海马及丘脑细胞膜 Ca2 、Mg2 - ATP酶活性的变化情况 ,用组织化学方法测定其活性。　结果　 1m W/ cm2时 ,皮层、海马及丘脑 Ca2 、Mg2 - ATP酶活性均比对照组高 (P<0 .0 5 ) ,5 m W/ cm2 时 ,酶活性与对照组差别均无显著性的意义 ,10 m W/ cm2 时 ,皮层、海马酶活性比对照组显著降低 ,而丘脑则无明显变化。　结论　 2 45 0 MHz微波照射小鼠时 ,脑组织细胞膜上 Ca2 、Mg2 -ATP酶活性随照射强度不同而有不同变化。受高强度照射时 ,参与学习记忆功能的皮层、海马先于参与体温调节功能的丘脑受到影响     

氦氧100m饱和－112m巡回潜水的医学保障

４名潜水员在甲板加压舱（ＤＣＣ）内１．１ＭＰａ氦氧饱和条件下暴露７２ｈ４ｍｉｎ，并分别经潜水钟（ＳＣＣ）到１１２ｍ深度作１５ｍｉｎ的巡潜。饱和潜水期间，ＤＣＣ内氧分压控制在４０ｋＰａ，氮分压低于１３６ｋＰａ，氦分压为９２５ｋＰａ，二氧化碳分压小于１０ｋＰａ。ＳＣＣ内氧分压为４５ｋＰａ，二氧化碳分压控制在１ｋＰａ以内。巡潜时潜水员呼吸氧分压为１１０ｋＰａ的氦氧混合气。减压按英国海军表修正方案。在潜水现场条件较差的情况下，未发生减压病、氧中毒、缺氧症和其它疾病；除有时晕船以外，潜水员生理状况和主观感觉良好，顺利完成了各项水下作业任务。     

Index of lipid peroxidation and glucose utilization in the cerebrospinal fluid in patients with cerebral infarction

Cerebral ischemia could be observed as acute metabolic crisis, when oxygen and glucose supply is compromised and synthesis of energy is insufficient. Apart from the excitotoxicity, increased production of reactive oxygen species with consequent lipid peroxidation is also included in neuronal cell damage. Furthermore, these toxic compounds could also be produced during the process of secondary inflammation of ischemic tissue. In the early stage of ischemia, as a systemic response to acute stress, there is an increase in glucose level in cerebrospinal fluid (CSF) and peripheral blood. According to the metabolic crisis and acidosis in ischemic brain tissue we investigated index of lipid peroxidation (ILP) and glucose utilization (IGU) in CSF of 53 patients of both sexes, aged 55-70 years with cerebral infarction. Control group comprised 15 patients with sudden onset of motor deficit subjected to diagnostic lumbar radiculography and suspected on discal genesis. ILP in CSF, as the indicator and sequela of neuronal cell membranes damage, was two fold increased in the acute period of cerebral infarction and maximal values (3.5 times) were noticed 24 hours after the ischemic episode compared to controls. Besides the increase in glucose concentration in peripheral blood and CSF of patients with cerebral infarction, IGU was decreased (37%) with minimal values (32%) 24 hours after the ischemia. These changes indicate that glucose is available but cells are incapable to metabolize it. We concluded that ILP and IGU in CSF of patients with cerebral infarction could be indicators of metabolic dysfunction and neuronal cell damage. Also, these results suggest the significance of polyvalent therapy including antioxidative and antiinflammatory agents in acute phase of cerebral ischemia.     

Effect of Electromagnetic Pulses (EMP) on associative learning in mice and a preliminary study of mechanism

Abstract

Purpose: To investigate the effects of electromagnetic pulses (EMP) on associative learning in mice and test a preliminary mechanism for these effects.

Materials and methods: A tapered parallel plate gigahertz transverse electromagnetic (GTEM) cell with a flared rectangular coaxial transmission line was used to expose male BALB/c mice to EMP (peak-intensity 400 kV/m, rise-time 10 ns, pulse-width 350 ns, 0.5 Hz and total 200 pulses). Concurrent sham-exposed mice were used as a control. Associative learning, oxidative stress in the brain, serum chemistry and the protective action of tocopherol monoglucoside (TMG) in mice were measured, respectively.

Results: (1) Twelve hour and 1 day post EMP exposure associative learning was reduced significantly compared with sham control (p < 0.05) but recovered at 2 d post EMP exposure. (2) Compared with the sham control, lipid peroxidation of brain tissue and chemiluminescence (CL) intensity increased significantly (p < 0.05), while the activity of the antioxidant enzymes Superoxide Dismutase [SOD], Glutathione [GSH], Glutathione Peroxidase [GSH-Px], Catalase [CAT]) decreased significantly (p < 0.05) at 3 h, 6 h, 12 h and 1 d post EMP exposure. All these parameters recovered at 2 d post EMP exposure. (3) No significant differences between the sham control group and EMP exposed group were observed in serum cholesterol and triglycerides. (4) Pretreatment of mice with TMG showed protective effects to EMP exposure.

Conclusions: EMP exposure significantly decreased associative learning in mice and TMG acted as an effective protective agent from EMP exposure. This mechanism could involve an increase of oxidative stress in brain by EMP exposure.     

茶多酚对重复+Gz暴露大鼠脑脂质过氧化反应和肝肾功能的影响

观察重复＋１０Ｇｚ暴露对大鼠脑脂质过氧化反应和肝肾功能的影响以及天然抗氧化剂茶多酚（ＴＰ）的防护作用。方法２４只雄性Ｗｉｓｔａｒ大鼠随机等分为三组（ｎ＝８）：Ａ组（对照组）,Ｂ组（＋１０Ｇｚ组）和Ｃ组（ＴＰ组）。Ｂ、Ｃ组重复＋１０Ｇｚ暴露（每次３０ｓ,Ｇ增长率约为０．５Ｇ／ｓ,３次／ｄ,间隔＋１Ｇｚ１ｍｉｎ,３ｄ／ｗｋ,共４ｗｋ）,而Ａ组仅受＋１Ｇｚ作用。Ｃ组于＋Ｇｚ实验前约１ｈ灌胃给予ＴＰ（２００ｍｇ／ｋｇ）,另外两组给予等量蒸馏水。测定脑脂质过氧化反应、肝肾功能和血脂水平。结果与对照组相比,Ｂ组大脑皮层匀浆、线粒体和胞浆脂质过氧化反应明显增强（Ｐ＜０．０５）,血浆肌酐水平明显升高（Ｐ＜０．０１）;而ＴＰ对此过氧化反应具有显著抑制作用并明显降低血浆肌酐水平。各组间血清谷丙转氨酶活性、甘油三酯和总胆固醇水平无统计学差异。结论重复高＋Ｇｚ作用可引起脑自由基损伤并损害肾功能,而天然抗氧化剂茶多酚具有明显的保护作用。     

原癌基因c-fos在大鼠急性局灶性脑缺血再灌注损伤和高压氧治疗后表达的变化

目的　探讨原癌基因 c- fos在大鼠急性局灶性脑缺血 /再灌注损伤和高压氧 (HBO)治疗后表达的变化。方法　用血管内细丝栓堵大鼠的大脑中动脉 (MCA ) ,制作成局灶性脑缺血动物模型 ,利用免疫组织化学方法 ,观察了 MCA缺血 1 h,再灌注 4、1 1、2 3、71 h c- fos癌基因表达的变化 ,在以上期间同时应用常压 0 .1 MPa纯氧或 0 .2 5 MPa HBO于开始缺血后 2、9、2 1、45和 6 9h分别治疗 1次 (1 h)。结果　缺血后 5 h,c- fos原癌基因在梗塞区皮层、纹状体、视前区均有明显表达 ,持续 1 2～ 2 4h后开始减弱 ,72 h基本消失。 HBO治疗后 ,各时间点 c- fos癌基因在上述区域的表达均明显减弱。结论　 HBO可明显抑制大鼠急性局灶性脑缺血 /再灌注损伤区 c- fos癌基因的表达