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缺血再灌注损伤改变了食指局部加热时的皮肤微血管反应。

Ischemia-reperfusion injury alters skin microvascular responses to local heating of the index finger.

机构信息

Environmental Ergonomics Laboratory, Department of Kinesiology, Brock University, St. Catharines, ON L2S 3A1, Canada.

Environmental Ergonomics Laboratory, Department of Kinesiology, Brock University, St. Catharines, ON L2S 3A1, Canada.

出版信息

Microvasc Res. 2018 Jul;118:12-19. doi: 10.1016/j.mvr.2018.02.003. Epub 2018 Feb 10.

Abstract

BACKGROUND

Ischemia-reperfusion (IR) injury impairs microcirculatory function by reducing nitric oxide (NO) bioavailability and increasing sympathetic tone. This study non-invasively examined the effects of acute upper limb IR injury on local thermal hyperemia (LTH) in glabrous and non-glabrous finger skin.

MATERIALS AND METHODS

In ten healthy males, LTH was examined twice (~7-10 d apart) for each skin type on the index finger using laser-Doppler flowmetry in a counterbalanced design with either 1) 20 min ischemia, followed by reperfusion (ISCH) or 2) time-matched control (SHAM). LTH tests were performed using a standard heating protocol (33-42 °C at 1 °C·20 s + 20 min at 44 °C) and baseline, initial peak, nadir, delayed plateau and maximal heating phases were identified as well as vasodilatory onset time and time to initial peak. Cutaneous vasomotion was evaluated using spectral analysis and comparing absolute and normalized wavelet amplitudes between conditions for both skin types at baseline and during LTH.

RESULTS

In non-glabrous skin, IR injury delayed the vasodilatory onset of local heating by 27.4 [11.3, 43.4] s (p = 0.004) and attenuated cutaneous vasodilation during the initial peak and sustained heating by -44.5 [-73.0, -15.9] PU (p = 0.003) and -34.4 [-62.9, -5.8] PU (p = 0.020), respectively. Analysis of normalized wavelet amplitudes in non-glabrous skin identified impaired microvascular function at baseline via NO-dependent mechanisms (-3.64 [-7.22, -0.05] %, p = 0.047), and during LTH via respiratory influences (-2.83 [-5.39, -0.21] %, p = 0.031). In glabrous skin, IR injury delayed vasodilatory onset time by 24.9 [1.1, 67.6] s (p = 0.042). The vasodilatory response to sustained local skin heating in glabrous skin was increased following IR injury (+56.3 [15.1, 116.5], p = 0.012), however, this was not evident when accounting for differences in blood pressure between conditions. Additionally, no other differences in vasodilatory or vasomotor functions were observed in this skin type between conditions (all, p > 0.05).

CONCLUSIONS

The current IR model elicits impaired cutaneous vasodilatory responses to local heating in young males, primarily in non-glabrous skin, and may be useful for exploring mechanisms of IR-injury and for testing potential countermeasures in otherwise healthy humans.

摘要

背景

缺血再灌注 (IR) 损伤通过降低一氧化氮 (NO) 的生物利用度和增加交感神经张力来损害微循环功能。本研究非侵入性地检查了急性上肢 IR 损伤对无毛和有毛手指皮肤局部热充血 (LTH) 的影响。

材料和方法

在 10 名健康男性中,使用激光多普勒流量metry 以平衡设计,在食指上两次(~7-10 d 之间)检查每种皮肤类型的 LTH,分别为 1)20 min 缺血,随后再灌注(ISCH)或 2)时间匹配的对照(SHAM)。LTH 测试使用标准加热方案(33-42°C 持续 20 s,然后 44°C 持续 20 min),并确定了基线、初始峰值、低谷、延迟平台和最大加热阶段,以及血管舒张起始时间和初始峰值时间。使用光谱分析评估皮肤血管运动,并比较两种皮肤类型在基线和 LTH 期间条件之间的绝对和归一化小波振幅。

结果

在无毛皮肤中,IR 损伤使局部加热的血管舒张起始延迟了 27.4 [11.3, 43.4] s(p=0.004),并在初始峰值和持续加热期间减弱了皮肤血管扩张-44.5 [-73.0, -15.9] PU(p=0.003)和-34.4 [-62.9, -5.8] PU(p=0.020)。在无毛皮肤中分析归一化小波振幅,发现通过 NO 依赖性机制在基线处存在微血管功能受损(-3.64 [-7.22, -0.05] %,p=0.047),并且在 LTH 期间通过呼吸影响受损(-2.83 [-5.39, -0.21] %,p=0.031)。在有毛皮肤中,IR 损伤使血管舒张起始时间延迟了 24.9 [1.1, 67.6] s(p=0.042)。在有毛皮肤中,持续局部皮肤加热的血管舒张反应在 IR 损伤后增加(+56.3 [15.1, 116.5],p=0.012),然而,当考虑到两种条件之间的血压差异时,这并不明显。此外,在这两种皮肤类型之间,条件之间的血管舒张或血管运动功能没有观察到其他差异(均,p>0.05)。

结论

当前的 IR 模型在年轻男性中引起局部热充血的皮肤血管舒张反应受损,主要在无毛皮肤中,可能有助于探索 IR 损伤的机制,并测试健康人潜在的对策。

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