奥拉西坦联合高压氧治疗重度一氧化碳中毒的疗效及对血清LPA、H-FABP及认知功能的影响

目的:探讨奥拉西坦联合高压氧治疗重度一氧化碳中毒的疗效及对血清溶血磷脂酸(LPA)、心型脂肪酸结合蛋白(H-FABP)及认知功能的影响。方法:选择2016年1月-2018年1月我院收治的重度一氧化碳中毒患者90例进行研究,以随机数表法分为观察组(n=48)和对照组(n=42)。对照组给予高压氧治疗,观察组在对照组的基础上加用奥拉西坦治疗。比较两组患者的临床疗效、血清LPA、H-FABP、认知能力、住院时间、迟发性脑病发生率。结果:两组总有效率分别为93.75%、76.19%,差异显著(P0.05);治疗前,两组血清LPA、H-FABP水平无显著性差异;治疗后,两组血清LPA、H-FABP均显著下降,且观察组血清LPA、H-FAB P水平低于对照组,(P0.05);治疗前,两组患者认知功能无显著性差异;治疗后,两组认知功能较治疗前均显著升高(P0.05),且观察组定向力、记忆力、注意力、语言能力水平均明显高于对照组(P0.05);观察组患者住院时间、迟发性脑病发生率均显著低于对照组,差异显著(P0.05)。结论:在重度一氧化碳中毒患者中应用奥拉西坦联合高压氧效果显著,可有效改善患者血清LPA、H-FABP水平及认知功能。     

HBO治疗对急性CO中毒后海马不同分区神经细胞凋亡的作用研究

目的:通过研究高压氧(HBO)治疗急性CO中毒大鼠海马不同分区神经细胞凋亡情况,探讨HBO治疗急性CO中毒的应用及机理。方法:利用雄性SD大鼠,建立急性CO中毒模型。应用免疫组织化学以及免疫荧光的方法,测定在染毒和CO中毒HBO治疗后1 d、3 d、7 d、14 d和21d Bcl-2、caspase-3、Neu N、BAX和MMP-9的表达水平的变化。结果:海马CA3区神经细胞对急性CO中毒与HBO治疗比CA1和CA2区更加敏感;急性CO中毒后,海马各区神经细胞凋亡程度随1 d、3 d、7 d、14 d和21 d时间延长而加重;BAX、caspase-3和Bcl-2等凋亡相关因子的表达水平与MMP-9的变化趋势一致:在1d开始增多,3d达到最大值,7d开始减少,14 d与21 d与正常组类似;CO中毒大鼠进行HBO治疗后,海马各区MMP-9、BAX、caspase-3和Bcl-2的表达水平明显降低;且HBO治疗7 d后,海马各区这些凋亡相关因子的表达降低最为明显。结论:海马CA3区神经细胞对急性CO中毒及HBO治疗敏感;海马神经细胞凋亡可能与神经细胞表达MMP-9降解神经细胞周围的基质,表达BAX、caspase-3和Bcl-2等凋亡相关因子促进凋亡发生有关;HBO治疗可降低MMP-9以及BAX、caspase-3和Bcl-2等凋亡因子的表达,抑制神经细胞的凋亡;HBO治疗7d对神经细胞凋亡的抑制作用最明显。     

醒脑静联合高压氧对急性一氧化碳中毒患者脑功能、肝肾功能及血清氧自由基的影响

摘要 目的：探讨醒脑静联合高压氧对急性一氧化碳中毒（ACOP）患者脑功能、肝肾功能及血清氧自由基的影响。方法：选取2017年1月至2020年1月期间我院收治的ACOP患者60例,按照随机数字表法将患者分为对照组（n=30）和研究组（n=30）,在常规治疗的基础上,对照组给予高压氧治疗,研究组给予醒脑静联合高压氧治疗,对比两组疗效、脑功能、肝肾功能、血清氧自由基以及平均苏醒时间、平均住院时间、迟发性脑病发生率。结果：研究组的临床总有效率为93.33%（28/30）,高于对照组的70.00%（21/30）（P<0.05）。两组治疗后天门冬氨酸氨基转移酶(AST)、丙氨酸氨基转移酶(ALT)、血肌酐(Scr)、血尿素氮(BUN)均较治疗前下降,且研究组低于对照组（P<0.05）。两组治疗后丙二醛 （MDA）较治疗前下降,且研究组低于对照组（P<0.05）;两组治疗后超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-PX）均较治疗前升高,且研究组高于对照组（P<0.05）。两组治疗后年龄相关性脑白质改变（ARWMC）分级量表、美国国立卫生研究院卒中量表(NIHSS)评分均较治疗前下降,且研究组低于对照组（P<0.05）;两组治疗后简易精神状态检查量表(MMSE)评分较治疗前升高,且研究组高于对照组（P<0.05）。研究组平均苏醒时间、平均住院时间均短于对照组,迟发性脑病发生率少于对照组（P<0.05）。结论：醒脑静联合高压氧治疗ACOP患者的疗效显著,有助于患者恢复,可有效清除其血清氧自由基,保护其脑功能、肝肾功能,减少迟发性脑病发生率。     

七叶皂苷钠对一氧化碳中毒迟发性脑病大鼠模型细胞凋亡 及调控凋亡基因表达的影响

目的:探讨七叶皂苷钠对一氧化碳中毒迟发性脑病大鼠模型细胞凋亡及Caspase-3表达的影响。方法:将30只大鼠随机分为正常对照组、一氧化碳中毒迟发性脑病大鼠模型对照组和七叶皂苷钠治疗组,原位末端标记法(TUNEL)检测细胞凋亡,免疫组化法检测Caspase-3的表达。结果:治疗组大鼠脑细胞凋亡率及Caspase-3表达较迟发性脑病对照组显著降低(P<0.01)。结论:七叶皂苷钠对一氧化碳中毒迟发性脑病的脑保护作用机制可能与干预脑细胞凋亡相关基因表达并减少神经细胞凋亡有关。     

核心稳定性训练联合高压氧对脑梗死恢复期患者血液流变学、脑能量代谢和血清NGF、NSE、MBP的影响

摘要 目的：观察核心稳定性训练联合高压氧对脑梗死恢复期患者血液流变学、脑能量代谢和血清神经生长因子（NGF）、神经元特异性烯醇化酶（NSE）、髓鞘碱性蛋白（MBP）的影响。方法：选择我院2018年3月~2021年3月期间收治的脑梗死恢复期患者103例。采用随机数字表法将患者分为对照组和观察组两组,例数分别为51例和52例。对照组患者接受核心稳定性训练,观察组患者接受核心稳定性训练联合高压氧治疗,对比两组疗效、血液流变学、脑能量代谢指标和血清NGF、NSE、MBP水平及相关量表评分。结果：观察组的临床总有效率高于对照组（P<0.05）。治疗后,两组上肢/下肢Lovett肌力评分升高,美国国立卫生研究院卒中量表（NIHSS）评分下降,且观察组的改变程度大于对照组（P<0.05）。治疗后,两组全血高切黏度、血细胞比容、全血低切黏度、血浆黏度下降,且观察组的改变程度大于对照组（P<0.05）。治疗后,两组血氧饱和度升高,空腹血糖、乳酸水平下降,且观察组的改变程度大于对照组（P<0.05）。治疗后,两组NGF水平升高,NSE、MBP水平下降,且观察组的改变程度大于对照组（P<0.05）。结论：核心稳定性训练联合高压氧应用于脑梗死恢复期患者,可促进其血液流变学、脑能量代谢改善,有效调节血清NGF、NSE、MBP水平,疗效明确。     

急性一氧化碳中毒131例临床分析

目的：探讨急性一氧化碳中毒（ACOP）患者的发病特点、临床表现及其对预后的影响。方法：回顾性分析2006年1月一2011年12月我院收治的131例ACOP患者,将其按病情的严重程度分为轻、中、重度3组,比较各组的发病原因和临床表现。结果：接触时间、基础疾病、血清肌酸激酶（CK）、昏迷时间在3组间差异有显著性（P〈0．01）,年龄、性别、中毒原因方面3组间差异无显著性（P〉0．05）。迟发性脑病组和无迟发性脑病组在年龄、基础疾病、并发症、接触时间、昏迷时间、CK方面差异有显著性（P〈0．01）;而在性别、中毒原因方面差异无显著性（P〉0．05）。结论：对于ACOP患者而言,接触时间长、伴有基础疾病、昏迷时间长、CK高不仅提示病情的严重程度,更是迟发性脑病的易患因素。而高压氧治疗是ACOP的首选及有效的治疗方法。     

Lipid Peroxidation was Involved in the Memory Impairment of Carbon Monoxide-induced Delayed Neuron Damage

Carbon monoxide (CO)-induced delayed neuron damage is the serious complication, but the underlying mechanisms are poorly understood. This study was designed to investigate the time-dependent changes of the lipid peroxidation (malondialdehyde, MDA) and antioxidative status (glutathione, GSH; glutathione peroxidase, GSH-Px; glutathione reductase, GR; and anti-reactive oxygen species anti-ROS) in nerve tissues for the possible mechanisms exploration. Adult rats were treated with CO by peritoneal injection, and sacrificed after day 0, 1, 3, 7, 14 and 21 of treatment. The results showed that the step-down latency progressively shortened while the numbers of error increased. Comparing with the level of day 0, MDA levels in serum, cerebral cortex and hippocampus significantly increased on day 1, 3 and 7. The level of GSH increased firstly but then decreased. The activities of GR, GSH-Px, and anti-ROS decreased in serum, cerebral cortex and hippocampus of rats after day 1, 3, 7, 14 and 21. Thus, we concluded that CO-mediated delayed neuron damage might be associated with elevation of lipid peroxidation and reduction of antioxidative status. The time-dependent changes of lipid peroxidation and antioxidative status in serum, cerebral cortex and hippocampus, at least in part, are involved in the toxic effects of CO poisoning on neuron.     

高压氧对急性CO 中毒大鼠脑内源性神经干细胞的影响

目的:探讨高压氧对急性CO中毒大鼠脑内源性神经干细胞的影响,分析HBO治疗急性CO中毒脑损伤的机制。方法:建立急性CO中毒大鼠模型,给予高压氧(HBO)治疗后,H-E染色观察大鼠脑组织病理学变化,免疫组织化学方法检测大鼠脑内神经干细胞(nestin)和星形胶质细胞(GFAP)的表达。结果:H-E染色标本上,对照组脑内神经元形态正常,染毒组脑皮质出现大量变性坏死细胞,海马锥体细胞层稀疏,HBO组坏死细胞明显减少。免疫组化结果显示对照组nestin和GFAP表达数量形态均正常,染毒组nestin表达增加,但无统计学意义,GFAP形态数量发生改变,HBO组nestin表达明显增加,且在大脑皮层可见部分nestin阳性细胞和nestin-GFAP双阳性细胞;GFAP表达趋于正常。结论:急性CO中毒作为脑损伤因素可轻度激活大鼠脑内源性神经干细胞,并使星形胶质细胞增生变形、神经元变性坏死,HBO治疗可减轻星形胶质细胞损伤,明显激活内源性神经干细胞,并促使其增殖、迁移和分化。提示HBO可能通过激活神经干细胞起治疗作用。     

高压氧联合地塞米松治疗突发性耳聋的疗效及对血液流变学的影响

目的:研究高压氧联合地塞米松治疗突发性耳聋的疗效及对血液流变学的影响。方法:选择2012年6月至2015年1月在我院接受治疗的突发性耳聋患者90例(124耳)进行研究。根据数字法随机分成观察组(45例,60耳)及对照组(45例,64耳),两组均给予常规的改善内耳微循环及神经营养类制剂治疗,对照组另给予地塞米松治疗,观察组在对照组基础上另给予高压氧治疗,治疗1个疗程后对比两组疗效,听力改善程度以及血液流变学指标变化。结果:观察组的总有效率是98.33%,显著高于对照组的89.06%,差异有统计学意义(P0.05)。治疗后观察组的听力损失程度显著优于对照组,纯音听阈显著低于对照组,差异有统计学意义(P0.05)。治疗后观察组的高切粘度、中切粘度、低切粘度、红细胞聚集指数均分别显著低于对照组,红细胞变形指数显著高于对照组,差异均有统计学意义(均P0.05)。结论:高压氧联合地塞米松治疗突发性耳聋患者具有更为显著的疗效,且可有效改善患者的血液流变学指标,值得临床推荐。     

Effects of Hyperbaric Oxygen at 1.25 Atmospheres Absolute with Normal Air on Macrophage Number and Infiltration during Rat Skeletal Muscle Regeneration

Use of mild hyperbaric oxygen less than 2 atmospheres absolute (2026.54 hPa) with normal air is emerging as a common complementary treatment for severe muscle injury. Although hyperbaric oxygen at over 2 atmospheres absolute with 100% O₂ promotes healing of skeletal muscle injury, it is not clear whether mild hyperbaric oxygen is equally effective. The purpose of the present study was to investigate the impact of hyperbaric oxygen at 1.25 atmospheres absolute (1266.59 hPa) with normal air on muscle regeneration. The tibialis anterior muscle of male Wistar rats was injured by injection of bupivacaine hydrochloride, and rats were randomly assigned to a hyperbaric oxygen experimental group or to a non-hyperbaric oxygen control group. Immediately after the injection, rats were exposed to hyperbaric oxygen, and the treatment was continued for 28 days. The cross-sectional area of centrally nucleated muscle fibers was significantly larger in rats exposed to hyperbaric oxygen than in controls 5 and 7 days after injury. The number of CD68- or CD68- and CD206-positive cells was significantly higher in rats exposed to hyperbaric oxygen than in controls 24 h after injury. Additionally, tumor necrosis factor-α and interleukin-10 mRNA expression levels were significantly higher in rats exposed to hyperbaric oxygen than in controls 24 h after injury. The number of Pax7- and MyoD- or MyoD- and myogenin-positive nuclei per mm² and the expression levels of these proteins were significantly higher in rats exposed to hyperbaric oxygen than in controls 5 days after injury. These results suggest that mild hyperbaric oxygen promotes skeletal muscle regeneration in the early phase after injury, possibly due to reduced hypoxic conditions leading to accelerated macrophage infiltration and phenotype transition. In conclusion, mild hyperbaric oxygen less than 2 atmospheres absolute with normal air is an appropriate support therapy for severe muscle injuries.     

乙酰唑胺对氧惊厥潜伏期的影响

为探讨脑血流调节与氧惊厥的关系,在复制大鼠氧惊厥模型的基础上,采用行为学方法测定氧惊厥潜伏期,并测定不司部位脑组织氧化与抗氧化指标,采用腹腔注射不同剂量脑血管扩张药物乙酰唑胺,观察脑血管扩张对氧化状态以及氧惊厥潜伏期的影响。观察结果为:(1)与生理盐水组相比,乙酰唑胺200、20 mg/kg体重组腹腔给药后氧惊厥潜伏期(纯氧6 ATA暴露)明显缩短(P<0.01),乙酰唑胺2 mg/kg体重组无明显改变(P>0.05);(2)腹腔给乙酰唑胺(20 mg/kg体重)或生理盐水后,各组各部位脑组织GSH-PX无显著差异(P>0.05),但随暴露时间的延长,其活力呈现先升高后降低的趋势;与对照组相比,乙酰唑胺6min组和生理盐水16min组皮层丙二醛(maleic dialdehyde,MDA)含量均明显增多(P<0.01),乙酰唑胺16 min组海马MDA含量明显增多(P<0.01)。结果表明,乙酰唑胺可缩短氧惊厥潜伏期,加重脑组织氧化损伤。     

蛛网膜下腔移植脐血干细胞治疗一氧化碳中毒后迟发性脑病的临床研究

目的观察蛛网膜下腔途径移植脐血干细胞治疗一氧化碳中毒后迟发性脑病（DEACMP）的安全性及治疗效果。方法26例DEACMP患者,按治疗方式分两组,其中12例经脐血干细胞移植治疗为治疗组,14例经高压氧治疗为对照组,对每例患者在治疗前和治疗后进行MMSE评分、ADL评分及颅脑CT检查。所有患者连续随访1年,观察预后及有无不良反应。采用两样本t检验、方差分析及卡方检验进行统计学分析。结果治疗组患者在干细胞移植术中均无特殊不适感,术中及术后24h内生命体征平稳,无发热,无穿刺点感染、出血等,术后门诊随访,均未出现移植相关并发症。1年后治疗组患者MMSE评分为25．08±4．10,高于对照组11．7±10．33（t=4．199,P=0．0003）;治疗组ADL评分为93．33±13．37,高于对照组41．07±38．39（t=4．478,P=0．0002）,差异均有统计学意义。治疗组CT检查结果好转率为83．33％,对照组好转率为30．00％两组比较差异有统计学意义（Х^2=4．402,P=0．0359）;治疗组临床痊愈率为50．00％,对照组为7．69％,差异有统计学意义（Х^2=4．055,P=0．0442）;治疗组临床有效率为100．00％,对照组为50．00％差异有统计学意义（Х^2=5．866,P=0．0154）。结论脐血干细胞移植治疗DEACMP疗效优于高压氧治疗,是一种安全有效的生物治疗方法,应得到重视和深入的研究。     

石菖蒲及α-细辛醚对疲劳运动大鼠学习记忆的影响及其机制

目的:研究石菖蒲及其活性成分-α-细辛醚改善疲劳运动大鼠学习记忆的作用及其机制。方法:80只SD大鼠随机分为正常对照组(A)、单纯运动组(B)、运动+α-细辛醚低、中、高剂量组(C、D、E)、运动+石菖蒲低、中、高剂量治疗组(F、G、H),每组10只。并在疲劳运动开始前2 h分别以0.10、0.50和1.00 mgα-细辛醚,灌胃C、D、E组,以0.12、1.20和4.80 g. kg^-1. wt^-1石菖蒲提取物,灌胃F、G、H组。实验结束后采用水迷宫实验进行学习记忆检测,采用生化法检测SOD、NOS活性和MDA含量,免疫印迹法检测海马n NOS蛋白表达水平。结果:实验后E和H组大鼠逃避潜伏期、海马脑组织MDA含量低于B、C、D、F和G组;穿越平台次数、海马脑组织SOD和NOS活性、n NOS蛋白表达高于B、C、D、F和G组,P均<0.01。A、E、H组大鼠海马脑组织SOD活性依次为A> E> H组,而MDA含量则相反,P均<0.01; E组大海马脑组织NOS活性和n NOS蛋白表达低于A和H组,P<0.01或P...     

The influence of hyperbaric oxygen on hemorheological parameters in diabetic rats

The effect of hyperbaric oxygen (HBO2) treatment on hemorheological parameters of diabetic rats was investigated. This study is a placebo-controlled, in vivo animal study. 30 streptozocin-induced diabetic rats were divided into two groups; one group received hyperbaric oxygen treatment while the other did not. Hematological and hemorheological parameters were tested with blood samples collected directly from the heart using surgical procedures. Student t-tests with a type I (alpha) error at 0.05 was used to test any significant difference between means of the hematologic and hemorheological parameters of the control (CON) and the HBO2 groups. Compared with the placebo group, hyperbaric oxygen resulted in significant higher lipid peroxidation stress of the erythrocytes and resistance of erythrocytes to deformation in rats of the HBO2 group. Whole blood viscosities measured at shear rates of 5, 150 and 400 s(-1) were all higher for the rats in the HBO2 group than those for rats in the control group. In addition, the oxygen delivery index was found to be significantly lower in rats of the HBO2 group. Thus, our work demonstrates that hyperbaric oxygen treatment significantly changes the hemorheological parameters in diabetic rats.     

Does granulocyte colony stimulating factor have protective effects against carbon monoxide-induced apoptosis?

Carbon monoxide (CO) produced by incomplete combustion of hydrocarbons, has many toxic effects on different organs, especially the heart and brain that have greater demands for oxygen. The present study aimed to evaluate the protective effects of granulocyte colony stimulating factor (G-CSF) on apoptosis after CO poisoning in rats. Male Wistar rats were exposed to CO 1500 or 3000 ppm for 60 min. Single and multiple doses of G-CSF (10, 50, and 100 μg/kg) were administered to animals. After CO poisoning, carboxyhemoglobin concentration was measured, apoptotic cells were evaluated by TUNEL assay and caspase 3 activity was determined by immunofluorescence. Blood levels of carboxyhemoglobin significantly increased following exposure to both 1500 and 3000 ppm concentrations of CO. However, carboxyhemoglobin levels were significantly higher following exposure to CO 3000 ppm compared to CO 1500 ppm (p?<?0.05). Differences in caspase 3 activity between G-CSF and control groups were significant and G-CSF could decrease apoptosis following CO 3000 ppm poisoning (p?<?0.001). TUNEL assay showed that in rats treat with 5 doses of G-CSF 100 μg/kg, apoptosis was significantly ameliorated compared to control rats and sham (rats that were not exposed to CO) group (p?<?0.05). Concerning caspase 3 activity and apoptosis rate, the best results were found in rats exposed to 3000 ppm and treated with G-CSF 100 μg/kg. In this study, we confirmed that CO poisoning leads to cardiomyocytes apoptosis which could be significantly reduced by G-CSF treatment.     

用于脑缺血小鼠海马SOD1表达的改进灌注固定法

常规灌注固定法多用于兔和大鼠等较大动物,并存在一些不足。改进了灌注固定法流程、灌注溶液的配方、流速、用量以及灌注装置,将其用于在显微操作下制备的缺血再灌注C57BL/6N小鼠模型,并对其海马进行H.E染色和免疫组织化学SOD1基因表达。结果显示,改进的灌注固定法使组织切片结构更加清晰,海马免疫阳性神经元定位于胞浆。缺血再灌注组(24hI/R)海马神经元SOD1表达比假手术对照组(sham-o)减少,而高压氧治疗组(24hHBO)SOD1表达有所恢复。表明改进的灌注固定法用于缺血再灌注C57BL/6N小鼠海马SOD1基因表达效果良好,结果可靠。实验结果提示,高压氧的治疗机制之一可能是通过增加SOD1基因表达而实现的。     

高压氧预处理对急性减压所致的大鼠肺组织细胞凋亡及Bcl-2/Bax表达的影响

目的:探讨高压氧预处理对减压病大鼠肺组织细胞凋亡的影响相关蛋白表达的影响。方法:雄性SD大鼠24只,随机分为3组,正常对照组(NC group)、HBO预处理组(HBOP group)、减压组(DCS group),每组8只。连续进行HBO预处理5天后进行减压病模型制备,取左侧肺组织进行湿干重比值测定,右侧肺组织用于病理实验;HE染色观察肺组织病理学改变,免疫组织化学法标记Bcl-2、Bax、Caspase-3与MMP-9阳性细胞表达,并对bcl-2/bax值进行分析。结果:减压组肺组织Bax、Caspase-3与MMP-9阳性细胞数明显增加(P0.05),而Bcl-2阳性细胞表达减少(P0.05);高压氧预处理组与减压组相比,Bax、Caspase-3与MMP-9阳性细胞数明显减少(P0.05),而Bcl-2阳性细胞表达增加(P0.05);大鼠肺组织减压组与高压氧预处理组Bcl-2/Bax值较对照组明显降低(P0.05);与减压组相比,高压氧预处理组明显升高(P0.05)。结论:HBO预处理可以减轻减压对肺组织的病理损伤,减轻肺泡和支气管上皮细胞的变性坏死,抑制细胞凋亡,从而起到对减压病的保护作用。     

Simulated descent v dexamethasone in treatment of acute mountain sickness: a randomised trial.

OBJECTIVE--Evaluation and comparison of the therapeutic efficacy of a portable hyperbaric chamber and dexamethasone in the treatment of acute mountain sickness. DESIGN--Randomised trial during the summer mountaineering season. SETTING--High altitude research laboratory in the Capanna Regina Margherita at 4559m above sea level (Alps Valais). SUBJECTS--31 climbers with symptoms of acute mountain sickness randomly assigned to different treatments. INTERVENTIONS--One hour of treatment in the hyperbaric chamber at a pressure of 193 mbar or oral administration of 8 mg dexamethasone initially, followed by 4 mg after 6 hours. MAIN OUTCOME MEASURES--Symptoms of acute mountain sickness (Lake Louise score, clinical score, and AMS-C score) before one and about 11 hours after beginning the different methods of treatment. Permitted intake of mild analgesics before treatment and in the follow up period. RESULTS--After one hour of treatment compression with 193 mbar caused a significantly greater relief of symptoms of acute mountain sickness than dexamethasone (Lake Louise score: mean (SD) -4.6 (1.9) v -2.5 (1.8); clinical score: -4.0 (1.2) v -1.5 (1.4); AMS-C score: -1.24 (0.51) v -0.54 (0.59)). In contrast after about 11 hours subjects treated with dexamethasone suffered from significantly less severe acute mountain sickness than subjects treated with the hyperbaric chamber (-7.0 (3.6) v -1.6 (3.0); -4.1 (1.9) v -1.0 (1.5); -1.78 (0.73) v -0.75 (0.82) respectively). Intake of analgesics was similar in both groups. CONCLUSION--Both methods were efficient in treatment of acute mountain sickness. One hour of compression with 193 mbar in the hyperbaric chamber, corresponding to a descent of 2250 m, led to short term improvement but had no long term beneficial effect. On the other hand, treatment with dexamethasone in an oral dose of 8 mg initially followed by 4 mg every 6 hours resulted in a longer term clinical improvement. For optimal efficacy the two methods should be combined if descent or evacuation is not possible.     

Decompression sickness in the rat following a dive on trimix: recompression therapy with oxygen vs. heliox and oxygen.

Trimix (a mixture of helium, nitrogen, and oxygen) has been used in deep diving to reduce the risk of high-pressure nervous syndrome during compression and the time required for decompression at the end of the dive. There is no specific recompression treatment for decompression sickness (DCS) resulting from trimix diving. Our purpose was to validate a rat model of DCS on decompression from a trimix dive and to compare recompression treatment with oxygen and heliox (helium-oxygen). Rats were exposed to trimix in a hyperbaric chamber and tested for DCS while walking in a rotating wheel. We first established the experimental model, and then studied the effect of hyperbaric treatment on DCS: either hyperbaric oxygen (HBO) (1 h, 280 kPa oxygen) or heliox-HBO (0.5 h, 405 kPa heliox 50%-50% followed by 0.5 h, 280 kPa oxygen). Exposure to trimix was conducted at 1,110 kPa for 30 min, with a decompression rate of 100 kPa/min. Death and most DCS symptoms occurred during the 30-min period of walking. In contrast to humans, no permanent disability was found in the rats. Rats with a body mass of 100-150 g suffered no DCS. The risk of DCS in rats weighing 200-350 g increased linearly with body mass. Twenty-four hours after decompression, death rate was 40% in the control animals and zero in those treated immediately with HBO. When treatment was delayed by 5 min, death rate was 25 and 20% with HBO and heliox, respectively.     

石菖蒲及其活性成分-5-羟甲基糠醛对疲劳运动大鼠学习记忆的影响及其机制*

目的:研究石菖蒲及5-羟甲基糠醛(HMF)对疲劳运动大鼠学习记忆和海马ERK/CREB信号的影响。方法:将SD大鼠随机分为:正常组(A)、运动组( B )、运动+HMF低、中、高剂量组(C、D、E)、运动+石菖蒲低、中、高剂量组( F、G、H ),每组10只。 并在疲劳运动开始前2 h分别以0.10、1.00和3.00 mg. kg^-1. wt^-1 HMF,灌胃C、D、E组,以0.12、1.20和4.80 g. kg^-1. wt^-1石菖蒲提取物,灌胃 F、G、H组。实验结束后采用水迷宫实验进行学习记忆检测,用免疫印迹法测定海马p-ERK1/2和p-CREB表达。结果:E和H组大鼠逃避潜伏期低于B、C、D、F和G组;穿越平台次数、p-ERK1/2、p-CREB蛋白表达高于B、C、D、F和G组(P均＜0.01);除E组p-ERK2蛋白表达低于A、H组(P＜0.05)外,上述各指标A、E、H组比较,差异均无显著性(P均＞0.05)。结论:石菖蒲及HMF能明显改善运动疲劳大鼠学习记忆,其机制与上调海马ERK/CREB信号有关。