Department of Anesthesia, General Intensive Care and Pain Management, Medical University of Vienna, Vienna, Austria.
Department for Vascular Biology and Thrombosis Research, Centre for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Shock. 2021 Sep 1;56(3):384-395. doi: 10.1097/SHK.0000000000001728.
Supplemental oxygen is administered routinely in the clinical setting to relieve or prevent tissue hypoxia, but excessive exposure may induce oxidative damage or disrupt essential homeostatic functions. It is speculated that oxidative stress in leukocytes and platelets may contribute to vascular diseases by promoting inflammation and cell aggregation.
In this pilot study 30 healthy male volunteers (18-65 years) were exposed to high oxygen concentration (non-rebreather mask, 8 L/min, 100% O2) and synthetic air (non-rebreather mask, 8 L/min, 21% O2) in a cross-over design for 20 min at a 3-week interval. Venous blood samples were obtained at baseline and 1, 3, and 6 h postintervention. Primary outcome was generation of reactive oxygen species in leukocytes as measured by the redox-sensitive fluorescent dye dihydrorhodamine 123. Additional outcomes were oxidative stress in platelets and platelet aggregation as measured by thromboelastography (ROTEM) and Multiplate analyses.
High oxygen exposure induced oxidative stress in leukocytes as evidenced by significantly higher mean fluorescence intensity (MFI) compared with synthetic air at 3 h postintervention (47% higher, P = 0.015) and 6 h postintervention (37% higher, P = 0.133). Oxidative stress was also detectable in platelets (33% higher MFI in comparison with synthetic air at 6 h, P = 0.024; MFI 20% above baseline at 3 h, P = 0.036; 37% above baseline at 6 h, P = 0.002). ROTEM analyses demonstrated reduced mean clotting time 1 h postintervention compared with baseline (-4%, P = 0.049), whereas there were no significant effects on other surrogate coagulation parameters.
Clinically relevant oxygen exposure induces oxidative stress in leukocytes and platelets, which may influence the immune and clotting functions of these cells.
在临床环境中，常规给予补充氧气以缓解或预防组织缺氧，但过度暴露可能会诱导氧化损伤或破坏基本的体内平衡功能。据推测，白细胞和血小板中的氧化应激可能通过促进炎症和细胞聚集来导致血管疾病。
在这项初步研究中，30 名健康男性志愿者（18-65 岁）以交叉设计的方式在 3 周的间隔内，通过非再呼吸面罩（8 L/min，100% O2）和合成空气（非再呼吸面罩，8 L/min，21% O2）分别暴露于高氧浓度下 20 分钟。在干预后 1、3 和 6 小时采集静脉血样本。主要结局是通过氧化敏感荧光染料二氢罗丹明 123 测量白细胞中活性氧的产生。其他结局是通过血栓弹性描记术（ROTEM）和多板分析测量血小板中的氧化应激和血小板聚集。
与合成空气相比，高氧暴露在干预后 3 小时（增加 47%，P=0.015）和 6 小时（增加 37%，P=0.133）时白细胞中的氧化应激诱导明显更高的平均荧光强度（MFI）。血小板中的氧化应激也可检测到（与合成空气相比，6 小时时 MFI 增加 33%，P=0.024；3 小时时 MFI 比基线高 20%，P=0.036；6 小时时 MFI 比基线高 37%，P=0.002）。ROTEM 分析表明，与基线相比，干预后 1 小时的平均凝血时间缩短（减少 4%，P=0.049），但其他替代凝血参数没有显著影响。
临床相关的氧气暴露会导致白细胞和血小板中的氧化应激，这可能会影响这些细胞的免疫和凝血功能。
