Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Dallas, Dallas, Texas.
University of Texas Southwestern Medical Center, Dallas, Texas.
J Appl Physiol (1985). 2019 Dec 1;127(6):1511-1518. doi: 10.1152/japplphysiol.00290.2019. Epub 2019 Aug 15.
This study aimed to quantify the sedative effects, detection rates, and cardiovascular responses to xenon. On 3 occasions, participants breathed xenon (FXe 30% for 20 min; FXe 50% for 5 min; FXe 70% for 2 min) in a nonblinded design. Sedation was monitored by a board-certified anesthesiologist. During 70% xenon, participants were also verbally instructed to operate a manual value with time-to-task failure being recorded. Beat-by-beat hemodynamics were measured continuously by ECG, photoplethysmography, and transcranial Doppler. Over 48 h postadministration, xenon was measured in blood and urine by gas chromatography-mass spectrometry. Xenon caused variable levels of sedation and restlessness. Task failure of the self-operating value occurred at 60-90 s in most individuals. Over the first minute, 50% and 70% xenon caused a substantial reduction in total peripheral resistance ( < 0.05). All dosages caused an increase in cardiac output ( < 0.05). By the end of xenon inhalation, slight hypertension was observed after all three doses ( < 0.05), with an increase in middle cerebral artery velocity ( < 0.05). Xenon was consistently detected, albeit in trace amounts, up to 3 h after all three doses of xenon inhalation in blood and urine with variable results thereafter. Xenon inhalation caused sedation incompatible with self-operation of a breathing apparatus, thus causing a potential life-threatening condition in the absence of an anesthesiologist. Yet, xenon can only be reliably detected in blood and urine up to 3 h postacute dosing. Breathing xenon in dosages conceivable for doping purposes (FXe 30% for 20 min; FXe 50% for 5 min; FXe 70% for 2 min) causes an initial rapid fall in total peripheral resistance with tachycardia and thereafter a mild hypertension with elevated middle cerebral artery velocity. These dose duration intervals cause sedation that is incompatible with operating a breathing apparatus and can only be detected in blood and urine samples with a high probability for up to ~3 h.
本研究旨在量化氙气的镇静作用、检测率和心血管反应。在 3 次场合中，参与者以非盲法设计呼吸氙气（FXe30%20 分钟；FXe50%5 分钟；FXe70%2 分钟）。镇静作用由认证麻醉师监测。在 70%氙气时，参与者还被口头指示操作手动值，记录到任务失败的时间。通过心电图、光电容积描记法和经颅多普勒连续测量逐搏血液动力学。给药后 48 小时，通过气相色谱-质谱法测量血液和尿液中的氙气。氙气引起不同程度的镇静和不安。大多数个体的自我操作值任务失败发生在 60-90 秒。在最初的一分钟内，50%和 70%的氙气导致总外周阻力显著降低（<0.05）。所有剂量均导致心输出量增加（<0.05）。在氙气吸入结束时，所有三种剂量后都观察到轻微高血压（<0.05），大脑中动脉速度增加（<0.05）。尽管在所有三种剂量的氙气吸入后 3 小时后仍能检测到痕量的氙气，但此后的结果则有所不同。氙气吸入引起的镇静作用与呼吸装置的自我操作不兼容，因此在没有麻醉师的情况下可能导致危及生命的情况。然而，只有在急性给药后 3 小时内才能可靠地在血液和尿液中检测到氙气。以可能用于兴奋剂目的的剂量（FXe30%20 分钟；FXe50%5 分钟；FXe70%2 分钟）吸入氙气会导致总外周阻力迅速下降，伴心动过速，随后轻度高血压伴大脑中动脉速度升高。这些剂量-持续时间间隔会引起与操作呼吸装置不兼容的镇静作用，并且仅在血液和尿液样本中以高概率检测到，最长时间约为 3 小时。
