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副交感神经活动随着系统性硬化症的微血管损伤和血管内皮生长因子的增加而增加。

Parasympathetic activity increases with digital microvascular damage and vascular endothelial growth factor in systemic sclerosis.

机构信息

Department of Clinical Medicine, Scleroderma Unit, Sapienza University of Rome, Italy.

Department of Immuno-Rheumatology Unit, Campus Bio-Medico, University of Rome, Italy.

出版信息

Clin Exp Rheumatol. 2018 Jul-Aug;36 Suppl 113(4):24-27. Epub 2018 May 11.

PMID:29787366
Abstract

OBJECTIVES

The imbalance between angiogenic and angiostatic factors with derangement of the microvasculature are hallmarks of systemic sclerosis (SSc). Raynaud's phenomenon in SSc probably is due to the impaired neuroendothelial control mechanisms between vasoconstriction and vasodilatation. The aim of this study is to evaluate autonomic nervous system function using heart rate variability (HRV) analysis and to correlate with vascular endothelial growth factor (VEGF).

METHODS

Twenty-seven SSc patients were enrolled. HRV was measured and markers of global sympathetic and parasympathetic system, respectively standard deviation of normal-to-normal RR intervals (SDNN) and square root of the mean of the sum of the squares of differences between adjacent NN intervals (RMSSD) were evaluated. Serum VEGF levels and nailfold videocapillaroscopy (NVC) were performed.

RESULTS

A linear positive correlation was observed between RMSSD and VEGF (p<0.01, r=0.55), and RMSSD and disease duration (p< 0.01, r=0.54). The RMSSD median value was significantly increased (p< 0.05) with NVC damage progression. The RMSSD median value was significantly (p<0.05) higher in SSc patients with digital ulcers (DUs) than in SSc patients without DUs [44 (39.4-60.2) vs 24.6 (23-37.1)].

CONCLUSIONS

In our study parasympathetic modulation increases in relation to VEGF. When microcirculation is modified with capillaroscopic pattern progression and DUs, autonomic system seems to stimulate vasodilatation trough parasympathetic system. We can conclude that parasympathetic activity increases with digital microvascular damage and promotes VEGF release.

摘要

目的

血管生成和血管抑制因子失衡以及微血管紊乱是系统性硬化症(SSc)的特征。SSc 中的雷诺现象可能是由于血管收缩和血管舒张之间的神经内皮控制机制受损所致。本研究旨在通过心率变异性(HRV)分析评估自主神经系统功能,并与血管内皮生长因子(VEGF)相关联。

方法

共纳入 27 例 SSc 患者。测量 HRV,并评估总体交感和副交感系统的标志物,即正常-正常 RR 间期的标准差(SDNN)和相邻 NN 间期差值平方和的平方根(RMSSD)。进行血清 VEGF 水平和甲襞微血管检查(NVC)。

结果

RMSSD 与 VEGF 之间存在线性正相关(p<0.01,r=0.55),RMSSD 与疾病持续时间之间也存在线性正相关(p<0.01,r=0.54)。RMSSD 的中位数随着 NVC 损害的进展而显著增加(p<0.05)。与无 DUs 的 SSc 患者相比,有 DUs 的 SSc 患者的 RMSSD 中位数显著升高(p<0.05)[44(39.4-60.2)比 24.6(23-37.1)]。

结论

在我们的研究中,副交感神经调节随着 VEGF 的增加而增加。当微血管通过毛细血管模式进展和 DUs 发生变化时,自主神经系统似乎通过副交感神经系统刺激血管舒张。我们可以得出结论,副交感神经活动随着数字微血管损伤的增加而增加,并促进 VEGF 的释放。

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