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首页> 外文期刊>American Journal of Physiology >Endothelial function is impaired in the cutaneous microcirculation of adults with psoriasis through reductions in nitric oxide-dependent vasodilation
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Endothelial function is impaired in the cutaneous microcirculation of adults with psoriasis through reductions in nitric oxide-dependent vasodilation

机译：在通过减少一氧化氮依赖性血管沉积的情况下，在成人的皮肤微循环中损害内皮函数损害

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Psoriasis is an independent risk factor for cardiovascular disease; however, the underlying mechanisms are not fully understood. Deficits in conduit arterial function are evident in patients with psoriasis, but potential impairments in microcirculatory endothelial function remain unclear. We hypothesized that cutaneous microvascular dysfunction would be detectable in otherwise healthy individuals with psoriasis. Two intradermal microdialysis fibers were placed in (nonlesional) forearm skin of nine patients (3 men and 6 women, 39 ± 5 yr) with moderate (16 ± 2% of body surface area) plaque psoriasis and nine healthy (nonpsoriatic) control subjects (3 men and 6 women, 38 ± 5 yr) for local delivery of 1) lactated Ringer solution (control) and 2) 10 mM L-ascorbate (a nonspecific antioxidant). An index of skin blood flow was measured using laser-Doppler flowmetry during local heating (42°C). Nitric oxide (NO)-dependent vasodilation was directly quantified after perfusion of the nonspecific NO synthase inhibitor N~G-nitro-L-arginine methyl ester (15 mM). A third fiber was perfused with increasing concentrations (10~(-l0)- 10~(-2) M) of norepinephrine to elicit adrenoreceptor-mediated cutaneous vasoconstriction. NO-de-pendent vasodilation was attenuated in patients with psoriasis (57 ± 5% and 39 ± 1% maximum cutaneous vascular conductance in control subjects and adults with psoriasis, respectively, P < 0.01). L-Ascorbate did not improve NO-dependent vasodilation (P >0.05). There was no group difference in maximal vasoconstriction or micro-vascular sensitivity to norepinephrine (P >0.05). These data suggest that NO bioavailability is reduced in otherwise healthy individuals with psoriasis, which contributes to systemic microvascular dysfunction.
机译：牛皮癣是心血管疾病的独立危险因素;然而，潜在机制尚未完全理解。导管动脉功能的缺陷在牛皮癣患者中是明显的，但微循环内皮功能的潜在损伤仍然不清楚。我们假设皮肤微血管功能障碍将在具有牛皮癣的其他健康的个体中可检测到。将两种皮内微透析纤维置于九名患者（3名男性和6名女性，39±5 YR）中的（体面32％）中等（体表面积）斑块牛皮癣和九个健康（非六种）对照受试者（ 3名男子和6名女性，38±5 YR）用于局部递送1）乳酸林液（对照）和2）10 mm L-抗坏血酸（非特异性抗氧化剂）。在局部加热（42℃）期间使用激光多普勒流动测量皮肤血​​流指数。在灌注非特异性没有合成酶抑制剂N〜G-NITRO-L-精氨酸甲酯（15mM）后直接定量一氧化氮（NO）依赖性血管沉积。将第三纤维灌注核肾上腺素的浓度（10〜（-10） - 10〜（-2）m）以引发肾上腺蛋白介导的皮肤血管收缩。在牛皮癣患者中衰减了无裂缝血管舒张（57±5％和39±1％的控制受试者和具有牛皮癣的成年人的最高皮肤血管传导，P <0.01）。 L-抗坏血酸没有改善无依赖性血管舒张（P> 0.05）。最大血管收缩或对去甲肾上腺素的微血管敏感性没有群体差异（P> 0.05）。这些数据表明，在具有牛皮癣的其他身体上没有减少生物利用度，这有助于系统性微血管功能障碍。

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