Skin blood flow and nitric oxide during body heating in type 2 diabetes mellitus.

Skin blood flow and nitric oxide during body heating in type 2 diabetes mellitus.
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2 型糖尿病身体发热期间的皮肤血流量和一氧化氮。

DOI:
10.1152/japplphysiol.91289.2008
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发表时间:
2009
期刊:
Journal of applied physiology (Bethesda, Md. : 1985)
影响因子:
--
通讯作者:
Charkoudian,Nisha
Charkoudian,Nisha
中科院分区:
--
文献类型:
--
作者:
Sokolnicki,LynnA;Strom,NicholasA;Roberts,ShellyK;Kingsley-Berg,ShirleyA;Basu,Ananda;Charkoudian,Nisha

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2 型糖尿病 (T2DM) 患者经常表现出微血管功能障碍,可能导致体温调节受损,但潜在机制仍不清楚。我们的目标是量化 T2DM 患者与年龄相仿的非糖尿病对照受试者在身体发热期间的皮肤血流反应和一氧化氮介导的血管舒张。我们测量了 10 名 T2DM 患者和 14 名对照受试者在 45-60 分钟的全身加热 (WBH) 期间的皮肤血流量(激光多普勒血流测定法),并结合 NG-硝基-L-精氨酸甲酯(L-NAME;一氧化氮合酶抑制剂)或载体的皮内微透析。在每组的六名个体中,我们还通过对侧前臂的静脉阻塞体积描记法测量了前臂血流量(FBF)。 FBF 反应显示 T2DM 组在 WBH 期间绝对皮肤血管舒张减弱(PANOVA < 0.01;对照组峰值 FBF 13.1 ± 1.7 对比 T2DM 9.0 ± 1.6 ml·100 ml−1·min−1)。然而,一氧化氮对皮肤血管舒张反应的相对贡献(表示为最大皮肤血管电导的百分比)在各组之间没有差异(P>0.05)。我们得出的结论是,T2DM 个体的皮肤血管舒张剂对 WBH 的反应减少,但一氧化氮对这种较小的血管舒张的贡献在 T2DM 和对照个体之间是相似的。皮肤血管舒张的减少可能是 T2DM 体温调节受损的重要原因。
Individuals with type 2 diabetes mellitus (T2DM) often exhibit microvascular dysfunction that may contribute to impaired thermoregulation, but potential mechanisms remain unclear. Our goals were to quantify skin blood flow responses and nitric oxide-mediated vasodilation during body heating in individuals with T2DM compared with nondiabetic control subjects of similar age. We measured skin blood flow (laser-Doppler flowmetry) in conjunction with intradermal microdialysis ofNG-nitro-l-arginine methyl ester (l-NAME; nitric oxide synthase inhibitor) or vehicle during 45–60 min of whole body heating (WBH) in 10 individuals with T2DM and 14 control subjects. In six individuals from each group, we also measured forearm blood flow (FBF) by venous occlusion plethysmography on the contralateral forearm. FBF responses showed diminished absolute cutaneous vasodilation during WBH in the T2DM group (PANOVA< 0.01; peak FBF in control 13.1 ± 1.7 vs. T2DM 9.0 ± 1.6 ml·100 ml−1·min−1). However, the relative contribution of nitric oxide to the cutaneous vasodilator response (expressed as % of maximal cutaneous vascular conductance) was not different between groups (P> 0.05). We conclude that cutaneous vasodilator responses to WBH are decreased in individuals with T2DM, but the contribution of nitric oxide to this smaller vasodilation is similar between T2DM and control individuals. This decrease in cutaneous vasodilation is likely an important contributor to impaired thermoregulation in T2DM.
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