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首页> 外文期刊>The Internet Journal of Neuromonitoring >Normobaric Hyperoxia Does Not Induce Significant Electroencephalogram Changes in Healthy Male Subjects
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Normobaric Hyperoxia Does Not Induce Significant Electroencephalogram Changes in Healthy Male Subjects

机译：正常人高氧血症不会导致健康的男性受试者发生明显的脑电图变化。

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ObjectiveHyperoxia can cause slowing and epileptic seizures in the electroencephalogram (EEG) when administered under hyperbaric conditions. Also hyperventilation and ensuing hypocapnia induce EEG slowing and may provoke epileptiform acitivity in patients with epilepsy. We aimed to study whether prolonged normobaric hyperoxia without hyperventilation has any effects on EEG. Methods Ten healthy, non-smoking men, aged 21-30 years, were recruited. Nineteen-channel-EEG was recorded continuously during breathing of 100 % oxygen through a tight 5 cmH2O continuous positive airway pressure –mask for one hour resulting in a mean end-tidal oxygen concentration of 91.1% (SD 1.8%). EEG-signal was analysed both visually and quantitatively after Fast Fourier Transformation. Total power and main frequency band powers (beta, alpha, theta, and delta) were calculated from the power spectrum, and compared between the baseline (before starting 100% oxygen) and after one hour breathing of pure oxygen. ResultsA slight reduction in posterior alpha band power and a simultaneous increase in anterior and lateral slow EEG activity occurred during oxygenation, but none of the changes remained significant after adjustment for multiple statistical comparisons. No epileptiform or other adverse activity occurred in the EEG. ConclusionsIn healthy subjects, normobaric oxygen, even when administered in high concentrations, does not cause significant EEG slowing or produce any other, possibly harmful changes in the EEG. Introduction Hyperoxic ventilation (>21 % O2) is a widely used method in medical practice, for example in intensive care units and emergency departments. Despite the objective to improve tissue oxygen delivery, hyperoxia can paradoxically hinder oxygen supply to the brain. The mechanism is thought to be mediated via so called Haldane effect, i.e. reduced CO2- carrying capacity of oxyhemoglobin in association with high concentrations of physically dissolved O2. This leads to an increase in arterial CO2 which induces hyperventilation, followed by a decrease in CO2, and the ensuing hypocapnia causes vasoconstriction. Subsequent reduction in cerebral blood flow (CBF) is not, however, normalized by eliminating the hypocapnia (1).It is well known that normoxic hyperventilation induces slowing of electroenecphalographic (EEG) activity, although the general mechanisms behind this slowing have not yet been settled (1,2,3,4). The prevailing hypoxia theory suggests that the general slowing of the EEG during normoxic hyperventilation results from hypocapnia which initiates vasoconstriction and consequently decreases CBF causing cerebral hypoxia. However, a slight physiological decrease in CBF, such as that occurring during hyperventilation, does not alone cause slowing in EEG (5). On the other hand, it is known that hyperbaric oxygen (HBO) can cause EEG slowing and seizures (6). It has been demonstrated that EEG power in beta, delta and theta frequency bands increases during HBO, and before seizures there is an increase in theta activity and slowing in alpha rhythm (6). In an experimental study, Sato et al. showed (7) that HBO increases CBF and nitric oxide production before epileptiform EEG discharges occur.As a part of an anaesthesia research project using xenon gas for single-agent anaesthesia we had a unique opportunity to investigate the isolated effect of excessive hyperoxygenation in normobaric conditions and with normal breathing on EEG in healthy subjects. The oxygenation with 100% oxygen was performed for denitrogenation before anesthesia induction with xenon. The aim of the present study was to investigate the central nervous system (CNS) effects of pure normobaric hyperoxia by means of analysing the classical EEG power spectral variables. Methods The Ethical Committee of the Hospital District of Southwest Finland (Turku, Finland) approved the study protocol and after giving written informed consent, 10 healthy (American Society of Anaesthesiologi
机译：目的在高压条件下服用高氧血症可导致脑电图（EEG）缓慢和癫痫发作。过度换气和随之而来的低碳酸血症也会导致脑电图的减慢，并可能激发癫痫患者的癫痫样活动。我们旨在研究延长的常压高氧而不过度换气对脑电图是否有任何影响。方法招募了10名年龄在21-30岁之间的健康，禁烟的男性。在5 cmH2O连续正气道正压通气面罩呼吸100％氧气的过程中，连续记录了19个通道的EEG，持续1个小时，潮气末的平均氧气浓度为91.1％（标准偏差为1.8％）。快速傅里叶变换后，通过视觉和定量分析EEG信号。从功率谱计算总功率和主频带功率（β，α，θ和增量），并在基线（开始使用100％氧气之前）和呼吸一小时纯氧气后进行比较。结果在充氧过程中，后α带功率略有降低，同时前，外侧脑电图缓慢活动增加，但经过多次统计学比较调整后，这些变化均未见明显变化。脑电图中未出现癫痫样或其他不良活动。结论在健康受试者中，常压氧气即使以高浓度给药也不会引起脑电图明显减慢或产生任何其他可能有害的脑电图变化。简介高氧通气（> 21％O2）是医学实践中广泛使用的方法，例如在重症监护室和急诊室。尽管目标是改善组织氧的输送，但是高氧会自相矛盾地阻碍向大脑的氧供应。认为该机制是通过所谓的Haldane效应来介导的，即与高浓度的物理溶解的O2结合，降低了氧合血红蛋白的CO2携带能力。这导致动脉CO2增加，导致过度换气，然后CO2减少，随后的低碳酸血症引起血管收缩。然而，随后的脑血流量减少并未通过消除低碳酸血症而恢复正常（1）。众所周知，高氧通气会导致脑电图（EEG）活性减慢，尽管这种减慢的一般机制尚未被发现。定居（1,2,3,4）。普遍的缺氧理论表明，在常氧性换气过度期间脑电​​图的总体减慢是由低碳酸血症引起的，低碳酸血症引起血管收缩，从而降低了导致脑缺氧的CBF。但是，CBF的生理性轻微降低（例如过度换气期间的降低）并不能单独导致脑电图的减慢（5）。另一方面，已知高压氧（HBO）会导致脑电图减慢和癫痫发作（6）。已经证明，在HBO期间，β，δ和theta频带中的EEG功率会增加，在癫痫发作之前，θ活性会增加，α节律会减慢（6）。在一项实验研究中，佐藤等人。证明（7）HBO会在癫痫样脑电图放电发生之前增加CBF和一氧化氮的产生。作为使用氙气进行单剂麻醉的麻醉研究项目的一部分，我们有一个独特的机会来研究在常压条件下过度过氧化的孤立作用健康受试者的脑电图正常呼吸。在用氙气诱导麻醉之前，先用100％的氧气进行脱氧。本研究的目的是通过分析经典EEG功率谱变量来研究纯常压高氧对中枢神经系统（CNS）的影响。方法西南芬兰医院区伦理委员会（芬兰图尔库）批准了研究方案，在获得知情同意后，10名健康者（美国麻醉学会）

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