Hypoxic modulation of nitric oxide (NO) production pathways in the cutaneous microvasculature and its interaction with cold-induced reflex vasoconstriction, independent of local cooling, has yet to be identified. This study assessed the contribution of NO to non-glabrous microvasculature perfusion during hypoxia and whole-body cooling with concomitant inhibition of NO synthase (NOS; via L-NAME) and the nitrite reductase, xanthine oxidase (via allopurinol), two primary sources of NO production. Thirteen volunteers were exposed to independent and combined cooling via water perfused suit (5ºC) and normobaric hypoxia (F_iO₂, 0.109 ± 0.002). Cutaneous vascular conductance (CVC) was assessed across four sites with intradermal microdialysis perfusion of 1) Lactated Ringers solution (control), 2) 20 mmol L-NAME 3) 10 µmol allopurinol, or 4) combined L-NAME/allopurinol. Effects and interactions were assessed via 4-way repeated measures ANOVA. Independently, L-NAME reduced (43%, p < 0.001), while allopurinol did not alter CVC (p = 0.5). Cooling decreased CVC (p = 0.001) and the reduction in CVC was consistent across perfusates (~30%, p = 0.9). Hypoxia increased CVC (16%, p = 0.01), with this effect abolished by L-NAME infusion (p = 0.04). Cold-induced vasoconstriction was blunted by hypoxia, yet importantly hypoxia increased CVC to a similar extent (39% at the Ringer site) irrespective of environmental temperature, thus no interaction was observed between cold and hypoxia (p = 0.1). L-NAME restored vasoconstriction during combined cold-hypoxia (p = 0.01). This investigation suggests that reflex cold-induced cutaneous vasoconstriction acts independently of NO suppression, while hypoxia-induced cutaneous vasodilatation is dependent on NOS derived NO production.

中文翻译：

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一氧化氮对皮肤微血管功能的依赖性取决于独立和联合的低氧冷暴露。

尚未确定皮肤微脉管系统中一氧化氮（NO）生成途径的低氧调节及​​其与冷诱导的反射性血管收缩的相互作用，而与局部冷却无关。这项研究评估了NO在缺氧和全身冷却过程中对无纤维微血管灌注的贡献，同时抑制了NO合酶（NOS；通过L-NAME）和亚硝酸还原酶黄嘌呤氧化酶（通过别嘌呤醇），这是NO的主要来源。没有生产。13名志愿者分别通过灌水服（5ºC）和常压低氧（F _i O ₂，0.109±0.002）。通过皮内微透析灌注，评估以下四个部位的皮肤血管电导（CVC）：1）乳酸林格氏液（对照），2）20 mmol L-NAME 3）10 µmol别嘌呤醇或4）L-NAME /别嘌呤醇组合。通过四向重复测量方差分析评估效果和相互作用。独立地，L-NAME降低（43％，p <0.001），而别嘌醇没有改变CVC（p = 0.5）。冷却降低了CVC（p = 0.001），而灌流液中CVC的降低是一致的（〜30％，p = 0.9）。缺氧会增加CVC（16％，p = 0.01），而通过L-NAME输注（p = 0.04）可以消除这种效应。缺氧使冷诱导的血管收缩变钝，但重要的是，无论环境温度如何，缺氧都会使CVC增幅达到相似的程度（在Ringer部位为39％），因此，在寒冷和缺氧之间未观察到相互作用（p = 0.1）。L-NAME在合并冷缺氧期间恢复了血管收缩（p = 0.01）。这项研究表明，反射性冷诱导的皮肤血管收缩作用独立于NO抑制，而低氧诱导的皮肤血管舒张则取决于NOS衍生的NO产生。