Extreme Environments Laboratory, School of Sport, Health and Exercise Science, University of Portsmouth, Portsmouth, UK.
Regional Occupational Health Team (ROHT) Catterick, Catterick Garrison, UK.
Exp Physiol. 2023 Mar;108(3):448-464. doi: 10.1113/EP090722. Epub 2023 Feb 20.
What is the central question of this study? Are biomarkers of endothelial function, oxidative stress and inflammation altered by non-freezing cold injury (NFCI)? What is the main finding and its importance? Baseline plasma [interleukin-10] and [syndecan-1] were elevated in individuals with NFCI and cold-exposed control participants. Increased [endothelin-1] following thermal challenges might explain, in part, the increased pain/discomfort experienced with NFCI. Mild to moderate chronic NFCI does not appear to be associated with either oxidative stress or a pro-inflammatory state. Baseline [interleukin-10] and [syndecan-1] and post-heating [endothelin-1] are the most promising candidates for diagnosis of NFCI.
Plasma biomarkers of inflammation, oxidative stress, endothelial function and damage were examined in 16 individuals with chronic NFCI (NFCI) and matched control participants with (COLD, n = 17) or without (CON, n = 14) previous cold exposure. Venous blood samples were collected at baseline to assess plasma biomarkers of endothelial function (nitrate, nitrite and endothelin-1), inflammation [interleukin-6 (IL-6), interleukin-10 (IL-10), tumour necrosis factor alpha and E-selectin], oxidative stress [protein carbonyl, 4-hydroxy-2-nonenal (4-HNE), superoxide dismutase and nitrotyrosine) and endothelial damage [von Willebrand factor, syndecan-1 and tissue type plasminogen activator (TTPA)]. Immediately after whole-body heating and separately, foot cooling, blood samples were taken for measurement of plasma [nitrate], [nitrite], [endothelin-1], [IL-6], [4-HNE] and [TTPA]. At baseline, [IL-10] and [syndecan-1] were increased in NFCI (P < 0.001 and P = 0.015, respectively) and COLD (P = 0.033 and P = 0.030, respectively) compared with CON participants. The [4-HNE] was elevated in CON compared with both NFCI (P = 0.002) and COLD (P < 0.001). [Endothelin-1] was elevated in NFCI compared with COLD (P < 0.001) post-heating. The [4-HNE] was lower in NFCI compared with CON post-heating (P = 0.032) and lower than both COLD (P = 0.02) and CON (P = 0.015) post-cooling. No between-group differences were seen for the other biomarkers. Mild to moderate chronic NFCI does not appear to be associated with a pro-inflammatory state or oxidative stress. Baseline [IL-10] and [syndecan-1] and post-heating [endothelin-1] are the most promising candidates for diagnosing NFCI, but it is likely that a combination of tests will be required.
本研究的核心问题是什么？非冻结性冷伤 (NFCI) 是否改变了内皮功能、氧化应激和炎症的生物标志物？主要发现及其重要性是什么？基线血浆 [白细胞介素-10] 和 [黏附素-1] 在 NFCI 患者和冷暴露对照参与者中升高。热挑战后 [内皮素-1] 的增加可能部分解释了 NFCI 患者疼痛/不适的增加。轻度至中度慢性 NFCI 似乎与氧化应激或促炎状态无关。基线 [白细胞介素-10] 和 [黏附素-1] 和加热后 [内皮素-1] 是诊断 NFCI 最有希望的候选物。
在 16 名慢性 NFCI (NFCI) 患者和匹配的冷暴露对照参与者 (COLD，n=17) 或无冷暴露对照参与者 (CON，n=14) 中，检查了炎症、氧化应激、内皮功能和损伤的血浆生物标志物。在基线时采集静脉血样，以评估内皮功能的血浆生物标志物（硝酸盐、亚硝酸盐和内皮素-1）、炎症 [白细胞介素-6 (IL-6)、白细胞介素-10 (IL-10)、肿瘤坏死因子-α和 E-选择素]、氧化应激 [蛋白质羰基、4-羟基-2-壬烯醛 (4-HNE)、超氧化物歧化酶和硝基酪氨酸] 和内皮损伤 [血管性血友病因子、黏附素-1 和组织型纤溶酶原激活物 (TTPA)]。全身加热后和单独足部冷却后立即采集血液样本，以测量血浆 [硝酸盐]、[亚硝酸盐]、[内皮素-1]、[IL-6]、[4-HNE] 和 [TTPA]。在基线时，与 CON 参与者相比，NFCI (P<0.001 和 P=0.015) 和 COLD (P=0.033 和 P=0.030) 患者的 [白细胞介素-10] 和 [黏附素-1] 升高。与 CON 相比，CON 中的 [4-HNE] 升高 (P=0.002) 和 COLD (P<0.001)。与 COLD 相比，NFCI 患者的 [内皮素-1] 加热后升高 (P<0.001)。加热后，NFCI 中的 [4-HNE] 低于 CON (P=0.032)，低于 COLD (P=0.02) 和 CON (P=0.015)。其他生物标志物在组间无差异。轻度至中度慢性 NFCI 似乎与促炎状态或氧化应激无关。基线 [白细胞介素-10] 和 [黏附素-1] 和加热后 [内皮素-1] 是诊断 NFCI 最有希望的候选物，但可能需要组合测试。
