Local ascorbate administration inhibits the adrenergic vasoconstrictor response to local cooling in the human skin.

Local ascorbate administration inhibits the adrenergic vasoconstrictor response to local cooling in the human skin.
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局部抗坏血酸给药抑制肾上腺素能血管收缩剂对人体皮肤局部冷却的反应。

DOI:
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发表时间:
2010
影响因子:
3.3
通讯作者:
F. Yamazaki
F. Yamazaki
中科院分区:
医学2区
文献类型:
--
作者:
F. Yamazaki

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局部冷却(LC)的非labraous皮肤引起血管收缩,通过肾上腺素和一氧化氮(NO)系统的清除。由于冷却增加了平滑肌细胞中的活性氧,并诱导α-肾上腺素能受体的敏感性增加,因此补充抗氧化剂可能会通过肾上腺素能和/或NO系统减弱对皮肤LC的血管收缩反应。为了验证这一假设,我们研究了急性L-抗坏血酸(Asc,10 mM)补充在人体皮肤上的血管收缩反应,LC在皮肤和NO合酶(NOS)抑制或肾上腺素能受体阻滞剂的影响。在一项由三部分组成的研究中,在健康志愿者的前臂部位植入微透析纤维、局部冷却器和激光多普勒血流(LDF)探头。将部位以-1 ℃/min从34 ℃冷却至24 ℃,并在24 ℃下保持20 min(第1和2部分)或30 min(第3部分)。在第1和第2部分LC的最后10分钟期间,进行全身冷却以增加交感血管收缩活性。皮肤血管传导性(CVC)计算为LDF与血压的比值,并相对于冷却前的基线值表示。各部分的处理如下:第1部分)未处理,Asc;第2部分)N(G)-硝基-L-精氨酸甲酯(L-NAME)抑制NOS,联合L-NAME + Asc;第3部分)育亨宾(YOH)+普萘洛尔(PRO)拮抗α和β肾上腺素能受体,并联合YOH + PRO + Asc。LC期间,Asc部位(-31 +/-4%)的CVC降低小于(P < 0.001)未治疗部位(-56 +/-5%)。LC诱导的CVC减少在L-NAME + Asc位点(-23 +/-8%)比在L-NAME位点(-43 +/-7%)小(P < 0.05)。LC诱导的CVC减少在PRO + YOH位点(-56 +/-3%)和PRO + YOH + Asc位点(-50 +/-3%)之间没有差异。这些研究结果表明,抗氧化剂的补充抑制血管收缩反应,直接冷却通过肾上腺素受体依赖性机制在人类皮肤。
Local cooling (LC) of nonglabrous skin causes vasoconstriction via the adrenergic and removal of nitric oxide (NO) systems. Since cooling increases reactive oxygen species in smooth muscle cells and induces increased sensitivity of alpha-adrenergic receptors, antioxidant supplementation may attenuate the vasoconstrictor response to skin LC via adrenergic and/or NO systems. To test this hypothesis, we examined the effects of acute L-ascorbate (Asc, 10 mM) supplementation in human skin on the vasoconstrictor responses to LC in skin with and without NO synthase (NOS) inhibition or adrenergic receptor blockade. In a three-part study, forearm sites were instrumented with microdialysis fibers, local coolers, and laser-Doppler flow (LDF) probes in healthy volunteers. Sites were cooled from 34 to 24 degrees C at -1 degrees C/min and maintained at 24 degrees C for 20 min (parts 1 and 2) or 30 min (part 3). During the last 10 min of LC in parts 1 and 2, whole body cooling was performed to increase sympathetic vasoconstrictor activity. Cutaneous vascular conductance (CVC) was calculated as the ratio of LDF to blood pressure and expressed relative to the baseline value before cooling. Treatments in each part were as follows: part 1) untreated, Asc; part 2) N(G)-nitro-L-arginine methyl ester (L-NAME) to inhibit NOS, combined L-NAME + Asc; part 3) yohimbine (YOH) + propranolol (PRO) to antagonize alpha- and beta-adrenergic receptors and combined YOH + PRO + Asc. CVC reduction during LC was smaller (P < 0.001) at Asc sites (-31 +/- 4%) than at untreated sites (-56 +/- 5%). LC-induced reduction in CVC was smaller (P < 0.05) at L-NAME + Asc sites (-23 +/- 8%) than at L-NAME sites (-43 +/- 7%). LC-induced reduction in CVC did not differ between at PRO + YOH sites (-56 +/- 3%) and at PRO + YOH + Asc sites (-50 +/- 3%). These findings suggest that antioxidant supplementation inhibits the vasoconstrictor response to direct cooling through an adrenoceptor-dependent mechanism in human skin.
DOI: 10.1152/jappl.1998.85.3.824
发表时间: 1998-09-01
影响因子: 3.3
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影响因子: --
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