Environmental, Occupational, Aging (Integrative) Physiology Laboratory, Haute Ecole Bruxelles-Brabant (HE2B), 1160 Brussels, Belgium.
Physical Activity Teaching Unit, Motor Sciences Department, Université Libre de Bruxelles (ULB), 1050 Brussels, Belgium.
Int J Environ Res Public Health. 2022 Apr 28;19(9):5394. doi: 10.3390/ijerph19095394.
Background: This study aimed to observe the effects of a fast acute ascent to simulated high altitudes on cardiovascular function both in the main arteries and in peripheral circulation. Methods: We examined 17 healthy volunteers, between 18 and 50 years old, at sea level, at 3842 m of hypobaric hypoxia and after return to sea level. Cardiac output (CO) was measured with Doppler transthoracic echocardiography. Oxygen delivery was estimated as the product of CO and peripheral oxygen saturation (SpO2). The brachial artery’s flow-mediated dilation (FMD) was measured with the ultrasound method. Post-occlusion reactive hyperemia (PORH) was assessed by digital plethysmography. Results: During altitude stay, peripheral oxygen saturation decreased (84.9 ± 4.2% of pre-ascent values; p < 0.001). None of the volunteers presented any hypoxia-related symptoms. Nevertheless, an increase in cardiac output (143.2 ± 36.2% of pre-ascent values, p < 0.001) and oxygen delivery index (120.6 ± 28.4% of pre-ascent values; p > 0.05) was observed. FMD decreased (97.3 ± 4.5% of pre-ascent values; p < 0.05) and PORH did not change throughout the whole experiment. Τhe observed changes disappeared after return to sea level, and normoxia re-ensued. Conclusions: Acute exposure to hypobaric hypoxia resulted in decreased oxygen saturation and increased compensatory heart rate, cardiac output and oxygen delivery. Pre-occlusion vascular diameters increase probably due to the reduction in systemic vascular resistance preventing flow-mediated dilation from increasing. Mean Arterial Pressure possibly decrease for the same reason without altering post-occlusive reactive hyperemia throughout the whole experiment, which shows that compensation mechanisms that increase oxygen delivery are effective.
本研究旨在观察快速急性上升到模拟高海拔地区对主要动脉和外周循环心血管功能的影响。
我们检查了 17 名年龄在 18 至 50 岁之间的健康志愿者，在海平面、3842 米低气压缺氧环境中和返回海平面后分别进行检查。使用多普勒经胸超声心动图测量心输出量（CO）。氧输送被估计为 CO 和外周血氧饱和度（SpO2）的乘积。肱动脉血流介导的扩张（FMD）用超声方法测量。通过数字容积描记法评估后阻断反应性充血（PORH）。
在高原停留期间，外周血氧饱和度下降（下降至预上升值的 84.9±4.2%；p<0.001）。没有志愿者出现任何与缺氧相关的症状。然而，心输出量（增加 143.2±36.2%，p<0.001）和氧输送指数（增加 120.6±28.4%，p>0.05）增加。FMD 下降（下降至预上升值的 97.3±4.5%；p<0.05），而 PORH 在整个实验过程中没有变化。观察到的变化在返回海平面并重新恢复正常氧合后消失。
急性暴露于低压缺氧导致氧饱和度下降和代偿性心率、心输出量和氧输送增加。预阻断血管直径增加可能是由于全身血管阻力降低，防止血流介导的扩张增加。平均动脉压可能因同样的原因下降，而整个实验过程中后阻断反应性充血没有改变，这表明增加氧输送的代偿机制是有效的。
