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首页> 外文期刊>The Internet Journal of Neuromonitoring >Cerebral Oxygenation At High Altitude: Reproducible Data After Acclimatisation At 5050 Meters During A Common Trekking Tour In The Nepal Himalayas
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Cerebral Oxygenation At High Altitude: Reproducible Data After Acclimatisation At 5050 Meters During A Common Trekking Tour In The Nepal Himalayas

机译：高海拔地区的脑氧合：在尼泊尔喜马拉雅山的一次普通徒步旅行中，在5050米的高度适应之后，可再现的数据

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Trekking at high altitudes (>2500 m above sea level) demands adequate acclimatisation to hypobaric hypoxia. When adaptation is insufficient, health is threatened by acute mountain sickness (AMS), high altitude cerebral edema and high altitude pulmonary edema, respectively. Regional cerebral oximetric values (rSO2) were measured in 27 adults (8 f, 19 m; mean age + SD group A: 39.5 + 11.2 years; group B: 44.8 + 14.9 years) during two different ascending routes to an altitude of 5050 m using an INVOS 5100 cerebral oximeter. The results showed reproducible data in both groups (49.0 < mean rSO2 < 55.0). There was a significant (p < 0.05; ANOVA, Tukey test) decrease compared to baseline values at a level of 133 m.Further studies are necessary to obtain data from the acute phase of hypobaric hypoxia and from persons with AMS. Indroduction High altitude, defined as heights between 2500 and 5300 m above sea level, can become dangerous to health because of increasing hypobaric hypoxia, especially when acclimatisation has been insufficient [1]. At an altitude of 5000 m oxygen partial pressure is reduced to about one-half compared to sea level and peripheral oxygen saturation (SaO2) in the healthy human body is reduced to values of about 75 % [2]. It is possible, that such decreases in SaO2 influence cerebral oxygenation, and may be an important key in developing acute mountain sickness (AMS) and high altitude cerebral edema (HACE). To our knowledge, only five studies concerning regional cerebral oxygenation (rSO2) at high altitude measured with transcranial near infrared spectroscopy (NIRS) exist. As expected, all authors found a decrease in rSO2, however the decrease was less pronounced than the changes in SaO2, which is supposed to be an unknown compensation mechanism of brain [3,4,5,6,7]. Nevertheless, results have to be interpreted carefully because of dissimilar measurement conditions (different altitudes, kind and rate of ascent, geographical location, temperature) and methods (Critikon 2020 system, INVOS 3100 and 5100 system). Based on the common opinion that the rate of ascent is a main factor for developing AMS [8], the goal of this study was to evaluate, whether various routes, with similar rates of ascent result in different or reproducible changes in brain oxygenation data. For the first time, this present study seeks measured rSO2 from two different trekking groups, who started from the same location (2850 m) and time, but ascended to an altitude of 5050 m using two different routes and returned back within 22 days (Fig. 1).
机译：在高海拔（海拔2500 m以上）徒步旅行需要对低压缺氧有足够的适应能力。当适应能力不足时，健康将分别受到急性高山病（AMS），高原脑水肿和高原肺水肿的威胁。在两个不同的上升路径至5050 m的上升路径中，对27位成年人（8 f，19 m;平均年龄+ SD组A：39.5 + 11.2岁; B组：44.8 + 14.9岁）测量了局部脑血氧饱和度（rSO2）。使用INVOS 5100脑血氧仪。结果显示两组均具有可重复的数据（49.0 <平均rSO2 <55.0）。与基线值相比，在133 m的水平上有显着的下降（p <0.05; ANOVA，Tukey检验）。需要进一步的研究以获取来自低压缺氧急性期和AMS患者的数据。引入高海拔地区被定义为海拔高度在2500至5300 m之间的高海拔地区，由于低压缺氧的加剧，可能对健康构成威胁，尤其是在适应能力不足的情况下[1]。与海平面相比，在5000 m的海拔高度上，氧气的分压降低到大约一半，健康人体中的外围氧饱和度（SaO2）降低到大约75％[2]。 SaO2的这种减少可能会影响大脑的氧合作用，并且可能是发展急性高山病（AMS）和高海拔脑水肿（HACE）的重要关键。据我们所知，仅有五项关于经颅近红外光谱法（NIRS）测量的高海拔区域脑氧合（rSO2）的研究。不出所料，所有作者都发现rSO2的减少，但这种减少的幅度不如SaO2的变化明显，SaO2的变化被认为是未知的大脑补偿机制[3,4,5,6,7]。但是，由于测量条件（海拔高度，上升的种类和速率，地理位置，温度）和方法（Critikon 2020系统，INVOS 3100和5100系统）不同而必须仔细解释结果。基于普遍认为上升速度是发展AMS的主要因素[8]，本研究的目的是评估各种途径，以相同的上升速度是否会导致大脑氧合数据发生不同或可再现的变化。本研究首次从两个不同的徒步旅行组中寻找测量的rSO2，他们从相同的位置（2850 m）和时间开始，但使用两条不同的路线上升到5050 m的高度，并在22天内返回（图5）。 1）。

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