Women with a history of preeclampsia have preserved sensory nerve-mediated dilatation in the cutaneous microvasculature.
Women with a history of preeclampsia have preserved sensory nerve-mediated dilatation in the cutaneous microvasculature.
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DOI：
10.1113/ep090177
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发表时间：
2022-03
影响因子：
2.7
通讯作者：
Stanhewicz AE
中科院分区：
文献类型：
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作者：
Pyevich M;Alexander LM;Stanhewicz AE
患有先兆子痫（PE）的女性表现出微血管内皮功能障碍，部分由减少的一氧化氮（NO）依赖性机制介导。皮肤局部加热诱导双相血管舒张反应：感觉神经介导的初始峰值，随后是持续的内皮依赖性平台。我们以前已经表明，内皮依赖性平台减弱PE。然而，尚不清楚感觉神经介导的初始峰是否同样衰减。因此，本研究的目的是检查先兆子痫病史对感觉神经介导的血管舒张的影响以及NO依赖性对该反应的贡献。我们假设，PE将有一个衰减的初始峰值和减少NO依赖性的贡献，这种反应相比，妇女的历史，血压正常的妊娠（HC）。9例HC（31± 4岁）和9例PE（28± 6岁）接受标准局部加热方案（42°C; 0.1°C·s-1）。将两个皮内微透析纤维放置在前臂腹侧的皮肤中，用于连续局部递送单独的乳酸林格氏液（对照）或用于抑制一氧化氮合酶（NOS）的15 mM NG-硝基-L-精氨酸甲酯（L-NAME）。通过激光多普勒血流仪（LDF）测量每个部位的红细胞流量。计算皮肤血管传导率（CVC=LDF/平均动脉压）并归一化至最大值（%CVCmax; 28 mM SNP +局部加热43°C）。两组间的初始峰值无差异（HC：79±8 vs PE：80±10%CVCmax; p=0.936）。NOS抑制减弱了HC（57±18%CVCmax; p=0.003）和PE（54±10%CVCmax; p=0.002）的初始峰值。然而，初始峰的NO依赖性部分无差异（HC：23±16 vs PE：24±9%; p=0.777）。在PE中，局部加热平台（HC：99±4 vs PE：88±7%CVCmax; p=0.001）和NO对平台的贡献（HC：31±9 vs PE：17±14%; p=0.02）减弱。各组间初始峰值的NO依赖性扩张与平台期的NO依赖性扩张之间无相关性（R2 = 0.005; P = 0.943）。患有先兆子痫的妇女表现出减弱的微血管内皮依赖性扩张。然而，在先兆子痫后感觉神经介导的血管舒张没有差异，这表明在这些妇女中，神经源性反应的NO依赖性血管舒张与内皮依赖性NO介导的血管舒张无关。
Women who have had preeclampsia (PE) demonstrate microvascular endothelial dysfunction, mediated in part by reduced nitric oxide (NO)-dependent mechanisms. Localized heating of the skin induces a biphasic vasodilation response: a sensory nerve-mediated initial peak, followed by a sustained endothelium-dependent plateau. We have previously shown that the endothelium-dependent plateau is attenuated in PE. However, it is unknown if the sensory nerve-mediated initial peak is similarly attenuated. Therefore, the purpose of this study was to examine the effect of preeclampsia history on sensory nerve-mediated vasodilation and the NO-dependent contribution to that response. We hypothesized that PE would have an attenuated initial peak and a reduced NO-dependent contribution to that response compared to women with a history of normotensive pregnancy (HC). Nine HC (31±4yrs) and 9 PE (28±6yrs) underwent a standard local heating protocol (42°C; 0.1°C·s−1). Two intradermal microdialysis fibers were placed in the skin of the ventral forearm for the continuous local delivery of Lactated Ringer’s alone (control) or 15mM NG-nitro-L-arginine methyl ester (L-NAME) for nitric oxide synthase (NOS)-inhibition. Red blood cell flux was measured at each site via laser-Doppler flowmetry (LDF). Cutaneous vascular conductance was calculated (CVC=LDF/mean arterial pressure) and normalized to maximum (%CVCmax; 28mM SNP + local heat 43°C). There were no differences in the initial peak between groups (HC: 79±8 vs PE: 80±10%CVCmax; p=0.936). NOS-inhibition attenuated the initial peak in both HC (57±18%CVCmax; p=0.003) and PE (54±10%CVCmax; p=0.002). However, there were no differences in the NO-dependent portion of initial peak (HC: 23±16 vs PE: 24±9%; p=0.777). The local heating plateau (HC: 99±4 vs PE: 88±7%CVCmax; p=0.001) and NO-contribution to the plateau (HC: 31±9 vs PE: 17±14%; p=0.02) were attenuated in PE. There was no relation between NO-dependent dilation in the initial peak and NO-dependent dilation in the plateau across groups (R2 = 0.005; P = 0.943). Women who have had preeclampsia demonstrate attenuated microvascular endothelium-dependent dilation. However, there are no differences in sensory nerve-mediated vasodilation following preeclampsia, suggesting that the NO-dependent vasodilation of the neurogenic response is not related to endothelium-dependent NO-mediated dilation in these women.