Effect of dietary vitamin E or selenium on prostaglandin dehydrogenase in hyperoxic rat lung

Weanling male rats were fed semi-purified diets supplemented with 0, 60, or 600 IU X g-1 vitamin E or 0, 100 or 1000 ppb selenium. One group was injected daily with vitamin E at a rate equivalent to consumption of 60 IU X kg-1. Animals from all groups were sacrificed after exposure to normobaric oxygen or air for 48 h. Lung tissue was analyzed for the combined activity of prostaglandin dehydrogenase and reductase. Using the decline in enzyme activity as an indicator of susceptibility to oxygen poisoning, protection against hyperoxia was directly related to the level of vitamin E supplementation. Selenium supplemented at 100 ppb provided significant protection when compared to 0 ppb or 1000 ppb. The latter dose may have been marginally toxic. We conclude that dietary supplementation of vitamin E and selenium may influence the relative susceptibility of an animal to pulmonary oxygen poisoning.     

Progression of and recovery from pulmonary oxygen toxicity in humans exposed to 5 ATA air

Animal studies suggest that pulmonary oxygen toxicity proceeds more slowly in diluted oxygen breathing mixtures than in pure oxygen at the same inspired partial pressure. We exposed 12 healthy subjects to air at 5 ATA (PiO2 = 1.05 ATA) in a hyperbaric chamber for 48 h, and compared the rate of development of symptoms of O2 toxicity to rates seen in previous studies using 100% O2 at 1 ATA. Symptoms consisted of chest tightness, cough, substernal discomfort, exertional dyspnea, anorexia, nausea and vomiting, headache and digital paresthesias starting at about 12 h, and continuing several days into the recovery period. Pulmonary function changes consisted of significant decrements in vital capacity, flow rates, and DLCO. Initial recovery was in a 0.50 ATA oxygen atmosphere, with the majority of subjects showing definite recovery in both symptoms and pulmonary function. Subjects showed complete recovery in about 8 d, although symptoms of fatigue and exertional dyspnea continued for a month in some cases. In contrast, none of the above changes were noted in an additional 6 subjects exposed to a 5 ATA environment with 6% oxygen (PiO2 = 0.30 ATA). No change in resting gas exchange, as indicated by alveolar-arterial oxygen gradients, was detected in either group. Comparison of these data to that for pure oxygen studies reveals no significant difference in the progression or character of pulmonary oxygen toxicity.     

Numerical chromosome abnormalities in 8-cell embryos generated from gamma-irradiated male mice in the absence and presence of vitamin E

PURPOSE: To investigate the effects of gamma-rays on male NMRI mice, in the absence or presence of vitamin E, on abnormalities in chromosome number in 8-cell embryos generated after mating with non-irradiated female mice. MATERIALS AND METHODS: The 8 - 11 week old male NMRI mice were irradiated whole body with 4 Gy of gamma-rays alone or in combination with 200 international units (IU)/kg vitamin E administered 1 h prior to irradiation. After 4 days, they were mated at weekly intervals with superovulated, non-irradiated female mice in successive 6 weekly periods. About 68 h post coitous (p.c.), 8-cell embryos were fixed on slides using standard methods in order to screen for abnormalities in chromosome number. RESULTS: In control embryos, 8% of metaphases were aneuploid whereas in embryos generated from irradiated mice, the frequency of aneuploidy increased dramatically at all post irradiation sampling times (p < 0.001). Administration of vitamin E one hour before irradiation, significantly decreased chromosomal aberrations in all 6 groups (p < 0.05). CONCLUSION: Data indicate that gamma-irradiation affects spermatogenesis and causes DNA alterations in sperm that may lead to chromosome abnormalities in subsequent embryos. Administration of vitamin E before irradiation effectively reduced the frequency of chromosomal abnormalities. The mechanism(s) by which vitamin E reduces genotoxic effects of radiation could be via radical scavenging or antioxidative effects.     

Numerical chromosome abnormalities in 8-cell embryos generated from γ-irradiated male mice in the absence and presence of vitamin E

Purpose:?To investigate the effects of γ-rays on male NMRI mice, in the absence or presence of vitamin E, on abnormalities in chromosome number in 8-cell embryos generated after mating with non-irradiated female mice.

Materials and methods:?The 8 – 11 week old male NMRI mice were irradiated whole body with 4 Gy of γ-rays alone or in combination with 200 international units (IU)/kg vitamin E administered 1 h prior to irradiation. After 4 days, they were mated at weekly intervals with superovulated, non-irradiated female mice in successive 6 weekly periods. About 68 h post coitous (p.c.), 8-cell embryos were fixed on slides using standard methods in order to screen for abnormalities in chromosome number.

Results:?In control embryos, 8% of metaphases were aneuploid whereas in embryos generated from irradiated mice, the frequency of aneuploidy increased dramatically at all post irradiation sampling times (p < 0.001). Administration of vitamin E one hour before irradiation, significantly decreased chromosomal aberrations in all 6 groups (p < 0.05).

Conclusion:?Data indicate that γ-irradiation affects spermatogenesis and causes DNA alterations in sperm that may lead to chromosome abnormalities in subsequent embryos. Administration of vitamin E before irradiation effectively reduced the frequency of chromosomal abnormalities. The mechanism(s) by which vitamin E reduces genotoxic effects of radiation could be via radical scavenging or antioxidative effects.     

Low temperature worsens mammalian oxygen toxicity

Oxygen toxicity was assessed in mice exposed to 5 ATA of oxygen. Central nervous system toxicity was measured as the latent period before convulsions, and lung damage estimated by wet and dry weight measurements. Our results confirmed previous findings that hyperbaric oxygen induces hypothermia in animals, and this effect is profound in mice exposed to 5 ATA of oxygen at ambient temperatures of 15 degrees C and 5 degrees C. However, even marked hypothermia had very little effect on the latent times to convulsions in mice. Unexpectedly, the combination of hypothermia and hyperbaric oxygen produced much more severe lung damage than either treatment alone, with a 2.7-fold increase in weight in the 5 degrees C group (average rectal temperature of 16.1 degrees C). These results indicate that hyperoxic-induced hypothermia cannot be considered a protective mechanism against oxygen toxicity and indeed hypothermia can markedly potentiate hyperbaric oxygen toxicity.     

Regional brain bioamine levels under hyperbaric oxygen in two unequally susceptible strains of mice

BACKGROUND: Hyperbaric oxygen (HBO) increases monoamine deamination with related toxic products which aggravates hyperbaric oxygen (HBO) neurotoxicity. However, the possibility of some protective action of monoamines balanced by the toxicity of their metabolites have received little attention. HYPOTHESIS: To try to unmask this protective action, we compared brain monoamine levels in two strains of mice differing in HBO-sensitivity and their sensitivity to HBO after norepinephrine (NE) depletion by N-(2-chloroethyl)-N-ethyl-2-bromo benzylamine (DSP4). METHODS: Mice were exposed to 6 ATA O2 for 90 min (C57 strain) and 24 min (HBO-sensitive CD1 strain) so that 50% of mice of each strain had preconvulsive symptoms when decompressed and 50%), had one generalized convulsion. After microwave sacrifice, monoamines in the cerebral cortex, the striatum and the brainstem were analyzed. Another series studied the effect of DSP4 on the delay to symptoms of these HBO)-exposed mice. RESULTS: NE normoxic levels in the striatum were greater in the HBO-sensitive CD1 than in the C57 strain. Under HBO, NE levels in the striatum and the cortex of CD1 fell without any concomitant increase in its metabolite whereas in the C57 strain, NE decreased less and its metabolite increased. There was no strain difference and little change in the NE levels in the brainstem. The increase in toxicity induced by DSP4 was highly significant in both strains; moreover C57 strain was more affected than CD1. CONCLUSION: Monoamine depletion before HBO aggravates HBO neurotoxicity. As monoamine deamination is known to be toxic, this demonstrates that monoaminergic activation is protective. The greater toxicity of DSP4 in the C57 strain suggests the involvement of monoamines in the strain-differential susceptibility to HBO. The lower sensitivity of CD1 mice to DSP4 may be related to a combination of less NE activation under HBO that in C57 and greater activation of peroxidation and amino acids in CD1 sensitive strain.     

游泳训练和高脂膳食对雄性大鼠发育中及成年后脂肪细胞数目的影响

目的:研究运动训练和高脂膳食两种因素对雄性大鼠生长发育过程中及成年后脂肪细胞数目的影响。方法:4周龄雄性SD大鼠随机分为普通饮食和高脂膳食两组,每组再分两个亚组:安静组和运动组,即普通饮食安静组(C组),普通饮食运动组(E组),高脂膳食安静组(H组)和高脂膳食运动组(HE组)。采用游泳运动,每次60分钟开始,递增至90分钟,3次/周。分别在干预4周、8周、12周后取材,完整剥离内脏脂肪组织,制备石蜡切片,测定脂肪细胞直径,计算脂肪细胞总数。结果:①4周时,HE组内脏脂肪组织重量显著高于E组;8周时,E组显著低于C组;12周时,H组高于C组和HE组,E组显著低于C组和HE组。8周和12周时,各组内脏脂肪重量均显著高于其对应4周组;12周时,除E组外,其它3组均高于其对应8周组。②4周时,H组内脏脂肪细胞直径大于C组和HE组;8周时,H组大于C组;12周时,E组小于C组和HE组,HE组小于H组。8周和12周时各组内脏脂肪细胞体积均大于4周时,12周时C组、H组和HE组均大于8周时。③4周时,各组间大鼠内脏脂肪细胞数目差异均无统计学意义;8周时,E组小于C组和HE组;12周时,H组大于C组和HE组。C组8周时大于4周时;H组12周时大于4周和8周时。以上差异均具有统计学意义,P<0.05或P<0.01。结论:高脂膳食提高雄性大鼠发育期脂肪细胞数目,运动训练可减弱高脂膳食提高脂肪细胞数目的作用。     

Incidence of oxygen toxicity during the treatment of dysbarism.

Oxygen (O2) toxicity may result from exposure to partial pressures of O2 above 0.6ATA. Potential toxic exposure for divers occurs during the treatment of dysbarism. In the recompression chamber, PO2 may range from 0.9ATA to 3.3ATA depending upon the treatment table employed. This retrospective study examines the nature and incidence of O2 toxicity in 998 patients who underwent recompression treatment at our facility from 1983 through 2001. Only patients evaluated for diving related injury were considered for this study. Of 1189 charts reviewed, 998 patients received recompression and were entered into this study. The total number of treatment exposures was determined as was the total number of O2 toxicity events characterized as either pulmonary or CNS, and patients were divided into male/female analysis. Overall incidence as well as the incidence for both toxicity types was determined, and their occurrence in both male and female patients was ascertained. 2166 recompressions were undertaken, 449 female and 1717 male. The peak PO2 for these treatments ranged from 2.6ATA to 2.9ATA. 155 O2 toxicity events occurred in 152 patients, 49 females and 103 males. Three patients, 2 females and 1 male, had mixed events. Incidence of an O2 toxic event = 7.0 per 100 recompressions. Incidence of pulmonary toxicity overall = 5.0 per 100 recompressions, while CNS events = 2.0 per 100 recompressions with overall seizure rate = 0.6 per 100 recompressions. In females, pulmonary toxicity rate = 6.9 per 100 recompressions, CNS toxicity rate = 4.4 per 100 recompressions with seizures occurring at 1.3 per 100 recompressions. In males, pulmonary toxicity rate = 4.6 per 100 recompressions, CNS toxicity rate = 1.4 per 100 recompressions, and seizures at 0.4 per 100 recompressions.     

Effects of vitamin E supplementation on oxidative stress at rest and after exercise to exhaustion in athletic students

AIM: The purpose of this study is to determine the effect following exercise to exhaustion of vitamin E supplementation on oxidative stress in athletic students. METHODS: Twenty male students voluntarily participated in the study and were randomly assigned (double blind) to either a vitamin E (daily dose of 450 mg of a-tocopherol for a period of 8 weeks) or a placebo group (took capsules containing 450 mg of lactose for 8 weeks). Before and after 8 weeks blood samples were collected at rest and after exercise to exhaustion. Oxidative stress markers were malondialdehyde (MDA), carbonylated proteins (CP) and creatine kinase (CK). Also, the effect of vitamin E on ergometer cycling time, as an example of endurance performance, was evaluated. RESULTS: ANOVA and independent t-tests indicated that vitamin E supplementation did not significantly change (P > 0.05) MDA, CP and CK values at rest, after exercise to exhaustion, and cycling time, but plasma volume after exercise to exhaustion significantly decreased (P < 0.05). CONCLUSIONS: Although vitamin E supplementation had no effect on exercise performance or capacity in athletic students, further investigation is required using larger numbers of subjects and measures of vitamin E before unequivocal conclusion can be stated.     

Vitamin E supplementation attenuates leakage of enzymes following 6 successive days of running training

The purpose of this study was to examine whether vitamin E supplementation in humans would attenuate an increase of serum enzymes as an indirect marker of muscle damage following a sudden large increase in the running distance in a 6-day running training or not. A randomized and placebo-controlled study was carried out on fourteen male runners who were supplied vitamin E (alpha-tocopherol 1200 IU x day(-1); E) or placebo (P) 4 weeks prior to (T1) and during 6 successive days of running training (48.3 +/- 5.7 km x day(-1), means +/- SD). Resting venous blood samples were obtained before maximal treadmill running, at T1, the day immediately before (T2), the next day (T3), and three weeks (T4) after the running training. Serum levels of alpha-tocopherol, lipid peroxidation products (thiobarbituric acid; TBA), creatine kinase (CK), lactate dehydrogenase (LDH), and LDH isozyme 1-5 were quantitatively analyzed. No significant difference was found in maximal oxygen uptake (VO2max) and maximal heart rates following the exhaustive exercise between the P and E group during the experiments. Vitamin E supplementation significantly increased serum alpha-tocopherol (p<0.001) and decreased TBA levels (p < 0.001) compared with pre-supplementation levels. Although serum CK and LDH activities increased significantly at T3 in either group, significantly lower CK (p < 0.05) and LDH (p < 0.001) levels were observed in the E group compared with the P group. The ratio of LDH1 to LDH2 (LDH1/LDH2) decreased significantly at T3 in either group compared with the T1 levels, since there was no significant difference in the LDH1/LDH2 between the P and E group throughout the experiments. These results indicate that vitamin E supplementation can reduce the leakage of CK and LDH following 6 successive days of endurance running. The protective effect of vitamin E against free radicals probably inhibits free-radical-induced muscle damage caused by a sudden large increase in the running distance.     

Treatment of Mycobacterium ulcerans infection by hyperbaric oxygenation.

Mycobacterium ulcerans causes chronic nectotizing ulcers of the skin and subcutaneous tissue and is a serious health problem in some tropical countries. Chemotherapy has not been effective, and the treatment of choice is extensive debridement followed by skin grafting. In spite of this, many infections are complicated by disfiguring scars, contraction deformities, and--rarely--amputation. There are other procedures that may promote healing (e.g., heat treatment, rifampicin), but none has been completely evaluated. In our study, hyperbaric oxygenation (HBO), an effective treatment for many bacterial diseases, including some mycobacterial infections, was used to treat mice with M. ulcerans-infected footpads. Three groups (40 mice/group) were treated daily with 100% oxygen by three different protocols: 2.5 ATA for 2 h; 2.5 ATA for 1.25 h, twice a day; and 2 ATA for 3.5 h. The degree of infection in the treated mice was compared weekly with 40 positive controls (infected, not treated). The HBO therapy was more effective in the group treated at 2.5 ATA for 1.25 h, twice a day. After 25 weeks, there had been two feet autoamputated and only 12 deaths among the mice, as compared to 18 feet amputated and 24 deaths in the control group. Thus, hyperbaric oxygenation has a beneficial effect in mice and, if used in conjunction with other therapeutic procedures in man, may be an effective therapeutic adjunct in treating M. ulcerans infections.     

Amphetamine as a protective agent against oxygen-induced convulsions in mice

Male mice exposed to hyperbaric oxygen (HBO) at 4.5 ATA O2 exhibit a number of toxic symptoms including convulsions, diminished respiration and an acoustic reaction controlled by the central nervous system. To study whether stimulation of the nervous system could offer protection against the convulsions, mice were injected i.p. with various doses of d-amphetamine before HBO. At a dose of 1.0 mg X kg-1 of d-amphetamine the mice could stay at 5 ATA O2 without convulsions about three times as long as those injected with saline only. At high doses, 4 and 8 mg X kg-1, there was a weak protective effect or the time to convulsions was shortened. Amphetamine increases the release of dopamine in the brain and it is possible that the mechanisms of protection against HBO induced convulsions are involved in that process. The degree of protection, however, depends on the dose; therefore, it also is supposed that amphetamine in low doses acts on the autoreceptors with a presynaptic effect, which in this case is protective against the convulsions without affecting the respiration.     

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。     

羔羊白肌病的诊断与防治

羔羊白肌病又称肌肉营养不良症,是由饲料或某些地区土壤中微量元素硒和维生素E缺乏或不足引起羔羊的一种代谢性疾病,临床特征为骨骼肌、心肌变性坏死,出现运动障碍及呼吸消化机能紊乱。该病病死率高,在新疆部分地区呈区域性分布,严重影响新疆肉羊产业的经济发展。本文对一例羔羊白肌病病例的临床症状、剖检变化和实验室诊断等内容进行了详细叙述,并对其防治措施进行了总结,供同行参考。     

硒缺乏和训练对雄性大鼠血清睾酮的影响

通过建立硒缺乏运动模型,结合游泳训练,观察硒缺乏和运动训练对雄性大鼠血清睾酮的影响。结果显示：①用低硒饲料喂养７周的大鼠的血清硒含量明显低于用补硒饲料喂养的大鼠。②缺硒安静大鼠的睾丸硒含量低于补硒安静大鼠,但降低的幅度比血清硒降低的幅度小,训练使缺硒大鼠的睾丸硒含量明显升高。③硒缺乏和训练均使大鼠的血清睾酮和游离睾酮水平降低,这种降低与血清的促性腺激素（ｒＬＨ和ｒＦＳＨ）水平无关,与睾丸Ｌｅｙｄｉｇ细胞膜上的ＬＨ／ｈＣＧ受体的亲和性及结合容量无关。④硒缺乏和训练均不影响血清的皮质酮水平,睾酮／皮质酮比值和游离睾酮／皮质酮比值的降低,主要是因为睾酮和游离睾酮的降低而引起的     

复合微量营养素对营养缺乏小鼠游泳耐力的影响及其机制

目的 研究复合微量营养素的抗疲劳效果及可能机制.方法 取SPF级雄性昆明种小鼠125只,分别以下述不同的饲料喂养.全营养素饲料.即AIN-93M饲料,主要成分和比例为:玉米淀粉46.6％、酪蛋白14％、糊精15.5％6.蔗糖10％、豆油4％、纤维素5％、矿物盐粉3.5％、维生素粉1％、胱氨酸0.18％、叔丁基氢醌8ppm.营养素缺乏饲料,在AIN-93M饲料的基础上将维生素粉和矿物盐粉减少为原来的70％、50％或30％(后称70％、50％、30％微量营养素饲料),其余以淀粉补足.复合微量营养素粉添加饲料,在营养素缺乏30％饲料的基础上,将减少的维生素粉和无机盐粉以复合微量营养素粉补足,其主要成分及含量(g/kg)为:VitA 0.25、VitB10.3、Vit B2 0.3、Vit B6 0.35、烟酸1.5、VitD 0.05、VitC50、VitE 10以及碳酸钙180、甘氨酸铁1、乳酸锌1、玉米淀粉755.25.分别干喂养14d和28d后取不同饲料(AIN-93M饲料及70％、50％、30％微量营养素饲料)喂养的小鼠,于尾部系5％体重的铅丝进行负重游泳,记录小鼠游泳力竭时间.于喂养至28d时,取不同饲料(AIN-93M饲料及70％微量营养素饲料、复合微量营养素粉添加饲料)喂养的小鼠,使其负重游泳60min,游泳后立即取外周血测定生化指标,取肝组织测定肝糖原含量.结果 与AIN-93M饲料喂养小鼠相比,30％微量营养素饲料喂养小鼠的摄食量显著减少(P＜0.05),50％和70％微量营养素饲料喂养小鼠的摄食量变化并不显著,但70％、50％、30％饲料喂养小鼠的负重游泳时间均显著缩短(P＜0.05).与AIN-93M饲料喂养小鼠相比,营养素缺乏饲料喂养的小鼠负重游泳时间显著缩短(P＜0.05),复合微量营养素粉饲料喂养小鼠游泳时间与营养素缺乏饲料喂养小鼠比较差异无统计学意义(P＞0.05),但延长了13.2％.小鼠游泳后生化指标的变化趋势主要表现为血糖和肝糖原水平下降.乳酸、游离脂肪酸(NEFA)和尿素氮(NPN)水平升高.营养素缺乏饲料喂养小鼠的前述变化更为明显,而复合微量营养素粉饲料可有效缓解营养缺乏所致血糖和肝糖原水平下降,下调血乳酸、NEFA和NPN水平.结论 微量营养素摄入不足对小鼠游泳耐力有明显影响,复合微量营养素具有一定的抗疲劳作用,其机制可能与运动过程机体能量代谢的调控有关.     

Changes in blood constituents in rats administered morphine and subjected to He-O2 at 11 ATA.

Changes in blood constituents in rats exposed to He-O2 at 1 ATA and 11 ATA after administration of morphine (100 mg/kg) are reported. Injected animals are compared with controls (non-injected) in ambient air and animals subjected to He-O2 at 1 ATA and 11 ATA. Temperature of the chamber was controlled and O2 partial pressure and CO2 levels were maintained at standard conditions. After morphine injection the rats were pressurized and maintained for 4 h before decompression, at which time additional blood samples were obtained. Morphine-injected animals in ambient air showed significant decreases in hematocrit, MCV, glucose, and protein in the blood while showing an increase in the leukocyte count and blood potassium. Non-injected animals maintained in He-O2 at 1 ATA and 11 ATA showed no deviation from ambient air control animals. Injected animals in He-O2 at 1 ATA showed no changes from those in ambient air, but animals injected and exposed to 11 ATA did not have a decreased serum protein level or an increase in potassium.     

Plasma volume and estimated liver plasma flow during hyperbaric and hyperoxic exposures in awake dogs

Five different experiments were conducted to determine if estimated liver plasma flow and/or plasma volume were changed as a result of exposure to 2.8 atmospheres absolute (ATA) while breathing 100% oxygen or 6 ATA while breathing compressed air. The experiments were designed to separate the relative roles of the ambient pressure, the partial pressure of oxygen, the time of high oxygen exposure or some combination of these factors on any observed changes. We found that time was not a factor in the changes seen. Hyperbaria resulted in a decrease in estimated liver plasma flow at all pressures greater than 1 ATA. There was an apparent increase in plasma volume at 1.3 ATA and a return towards 1 ATA values at higher pressures. Hyperoxia resulted in a decrease in estimated liver plasma flow at 975 mm Hg but not at 912 mm Hg. The flow was then increased again at 2128 mm Hg. Plasma volume decreased significantly at 912 mm Hg returned to baseline (152 mm Hg) values at 975 mm Hg and then decreased again at 1054 and 2128 mm Hg PO2.     

Tissue gas and blood analyses of human subjects breathing 80% argon and 20% oxygen.

Eight human volunteers, individually studied in a hyperbaric chamber, breathed: 1) air at 1 ATA; 2) 80% argon and 20% oxygen and 1 ATA for 30 min; 3) air at 1 ATA for 30 min; 4) 100% 02 at 1 ATA for 30 min; 5) air at 1 ATA for 30 min; 6) 100% O2 at 2 ATA for 60 min; and 7) 80% argon and 20% oxygen at 1 ATA for 30 min. Oxygen, carbon dioxide, nitrogen, and argon tensions were measured in muscle and subcutaneous tissue by mass spectroscopic analyses. Venous blood obtained at regular intervals was analyzed for coagulation and fibrinolytic factors. Inert gas narcosis was not observed. After breathing argon for 30 min, muscle argon tensions were almost three times subcutaneous tensions. Argon wash-in mirrored nitrogen wash-out. Argon wash-in and wash-out had no effect on tissue Po2 or Pco2. Coagulation and fibrinolytic changes usually associated with vascular bubbles were absent.     

高压氧联合艾塞那肽对高糖培养下视网膜神经节细胞保护作用

目的探讨高压氧联合艾塞那肽对高糖培养下视网膜神经节细胞(RGCs)的保护机制。方法传代培养RGC-5细胞系,分为对照组、高糖组、高压氧组、艾塞那肽组、高压氧联合艾塞那肽组。用CCK-8法检测高压氧、艾塞那肽对高糖培养下RGC-5细胞活性的影响,用流式细胞仪评估高压氧、艾塞那肽对高糖培养下RGC-5细胞凋亡的影响,通过电镜观察RGC-5细胞线粒体形态的变化。结果在1.4~2.2 ATA压力范围内,不同压力的高压氧预处理均可提高RGC-5细胞存活率,1.6 ATA压力是高压氧保护RGC-5细胞的最佳剂量。高压氧联合艾塞那肽可提高高糖培养下RGC-5细胞存活率,抑制RGC-5细胞凋亡。结论高压氧、艾塞那肽均能保护由高糖引起的RGC-5细胞的损害,而高压氧联合艾塞那肽的保护效果要比单纯高压氧治疗效果好。