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脑和肺对高氧低气压减压的生物标志物反应。

Brain and Lung Biomarker Responses to Hyperoxic Hypobaric Decompression.

出版信息

Aerosp Med Hum Perform. 2024 Sep 1;95(9):667-674. doi: 10.3357/AMHP.6391.2024.

DOI:10.3357/AMHP.6391.2024
PMID:39169490
Abstract

Biomarker responses to intensive decompression indicate systemic proinflammatory responses and possible neurological stress. To further investigate responses, 12 additional brain and lung biomarkers were assayed. A total of 15 healthy men (20 to 50 yr) undertook consecutive same-day ascents to 25,000 ft (7620 m), following denitrogenation, breathing 100% oxygen. Venous blood was sampled at baseline (T0), after the second ascent (T8), and next morning (T24). Soluble protein markers of brain and lung insult were analyzed by enzyme-linked immunosorbent assay with plasma microparticles quantified using flow cytometry. Levels of monocyte chemoattractant protein-1 and high mobility group box protein 1 were elevated at T8, by 36% and 16%, respectively, before returning to baseline. Levels of soluble receptor for advanced glycation end products fell by 8%, recovering by T24. Brain-derived neurotrophic factor rose by 80% over baseline at T24. Monocyte microparticle levels rose by factors of 3.7 at T8 and 2.7 at T24 due to early and late responses in different subjects. Other biomarkers were unaffected or not detected consistently. The elevated biomarkers at T8 suggest a neuroinflammatory response, with later elevation of brain-derived neurotrophic factor at T24 indicating an ongoing neurotrophic response and incomplete recovery. A substantial increase at T8 in the ratio of high mobility group box protein 1 to soluble receptor for advanced glycation end products suggests this axis may mediate the systemic inflammatory response to decompression. The mechanism of neuroinflammation is unclear but elevation of monocyte microparticles and monocyte chemoattractant protein-1 imply a key role for activated monocytes and/or macrophages.

摘要

生物标志物对强化减压的反应表明存在全身促炎反应和可能的神经应激。为了进一步研究反应,还测定了 12 种其他脑和肺生物标志物。总共 15 名健康男性(20 至 50 岁)在脱氮后连续同一天攀登到 25000 英尺(7620 米),呼吸 100%的氧气。在基线(T0)、第二次攀登后(T8)和次日早晨(T24)采集静脉血样。通过酶联免疫吸附试验分析脑和肺损伤的可溶性蛋白标志物,并使用流式细胞术定量测定血浆微粒。在 T8 时,单核细胞趋化蛋白-1 和高迁移率族蛋白 1 的水平升高,分别升高了 36%和 16%,然后恢复到基线。可溶性晚期糖基化终产物受体的水平下降了 8%,到 T24 时恢复。脑源性神经营养因子在 T24 时比基线升高了 80%。在 T8 和 T24,由于不同受试者的早期和晚期反应,单核细胞微粒的水平分别升高了 3.7 倍和 2.7 倍。其他生物标志物不受影响或未被一致检测到。T8 时升高的生物标志物提示存在神经炎症反应,T24 时脑源性神经营养因子升高表明存在持续的神经营养反应和不完全恢复。T8 时高迁移率族蛋白 1 与可溶性晚期糖基化终产物受体的比值显著升高,表明该轴可能介导减压引起的全身炎症反应。神经炎症的机制尚不清楚,但单核细胞微粒和单核细胞趋化蛋白-1 的升高表明激活的单核细胞和/或巨噬细胞可能发挥关键作用。

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