Aerosp Med Hum Perform. 2023 Oct 1;94(10):738-749. doi: 10.3357/AMHP.6247.2023.
Consistent blood biomarkers of hypobaric (altitude) decompression stress remain elusive. Recent laboratory investigation of decompression sickness risk at 25,000 ft (7620 m) enabled evaluation of early pathophysiological responses to exertional decompression stress. In this study, 15 healthy men, aged 20-50 yr, undertook 2 consecutive (same-day) ascents to 25,000 ft (7620 m) for 60 and 90 min, breathing 100% oxygen, each following 1 h of prior denitrogenation. Venous blood was sampled at baseline (T0), immediately after the second ascent (T8), and next morning (T24). Analyses encompassed whole blood hematology, endothelial microparticles, and soluble markers of cytokine response, endothelial function, inflammation, coagulopathy, oxidative stress, and brain insult, plus cortisol and creatine kinase. Acute hematological effects on neutrophils (mean 72% increase), eosinophils (40% decrease), monocytes (37% increase), and platelets (7% increase) normalized by T24. Consistent elevation (mean five-fold) of the cytokine interleukin-6 (IL-6) at T8 was proinflammatory and associated with venous gas emboli (microbubble) load. Levels of C-reactive protein and complement peptide C5a were persistently elevated at T24, the former by 100% over baseline. Additionally, glial fibrillary acidic protein, a sensitive marker of traumatic brain injury, increased by a mean 10% at T24. This complex composite environmental stress, comprising the triad of hyperoxia, decompression, and moderate exertion at altitude, provoked pathophysiological changes consistent with an IL-6 cytokine-mediated inflammatory response. Multiple persistent biomarker disturbances at T24 imply incomplete recovery the day after exposure. The elevation of glial fibrillary acidic protein similarly implies incomplete resolution following recent neurological insult.
目前仍难以找到低压（高原）减压应激的一致血液生物标志物。最近对 25000 英尺（7620 米）减压病风险的实验室研究，使人们能够评估运动性减压应激的早期病理生理反应。在这项研究中，15 名年龄在 20-50 岁的健康男性连续（同一天）两次攀登到 25000 英尺（7620 米），每次持续 60 和 90 分钟，呼吸 100%的氧气，每次都在之前的 1 小时内除氮。在基线（T0）、第二次攀登后立即（T8）和次日早晨（T24）采集静脉血样。分析包括全血血液学、内皮细胞微粒和细胞因子反应、内皮功能、炎症、凝血障碍、氧化应激和脑损伤、皮质醇和肌酸激酶的可溶性标志物。中性粒细胞（平均增加 72%）、嗜酸性粒细胞（减少 40%）、单核细胞（增加 37%）和血小板（增加 7%）的急性血液学效应在 T24 时正常化。细胞因子白细胞介素-6（IL-6）在 T8 时持续升高（平均升高五倍）呈炎症性，并与静脉气泡（微泡）负荷相关。C-反应蛋白和补体肽 C5a 的水平在 T24 时持续升高，前者比基线升高 100%。此外，胶质纤维酸性蛋白，一种敏感的外伤性脑损伤标志物，在 T24 时平均增加 10%。这种复杂的复合环境应激，包括高浓度氧、减压和中度在高原运动，引起了与 IL-6 细胞因子介导的炎症反应一致的病理生理变化。T24 时多个持续的生物标志物紊乱表明暴露后第二天恢复不完全。胶质纤维酸性蛋白的升高同样表明在最近的神经损伤后仍未完全解决。
