Vascular dysregulation in glaucoma: retinal vasoconstriction and normal neurovascular coupling in altitudinal visual field defects,EPMA Journal

当前位置： X-MOL 学术 › EPMA J. › 论文详情

Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)

Vascular dysregulation in glaucoma: retinal vasoconstriction and normal neurovascular coupling in altitudinal visual field defects
EPMA Journal ( IF 6.0 ) Pub Date : 2023-02-16 , DOI: 10.1007/s13167-023-00316-6
Wanshu Zhou ₁ , Bernhard A Sabel ₁

Affiliation

Purpose

Vision loss in glaucoma is not only associated with elevated intraocular pressure and neurodegeneration, but vascular dysregulation (VD) is a major factor. To optimize therapy, an improved understanding of concepts of predictive, preventive, and personalized medicine (3PM) is needed which is based on a more detailed understanding of VD pathology. Specifically, to learn if the root cause of glaucomatous vision loss is of neuronal (degeneration) or vascular origin, we now studied neurovascular coupling (NVC) and vessel morphology and their relationship to vision loss in glaucoma.

Methods

In patients with primary open angle glaucoma (POAG) (n = 30) and healthy controls (n = 22), NVC was studied using dynamic vessel analyzer to quantify retinal vessel diameter before, during, and after flicker light stimulation to evaluate the dilation response following neuronal activation. Vessel features and dilation were then related to branch level and visual field impairment.

Results

Retinal arterial and venous vessels had significantly smaller diameters in patients with POAG in comparison to controls. However, both arterial and venous dilation reached normal values during neuronal activation despite their smaller diameters. This was largely independent of visual field depth and varied among patients.

Conclusions

Because dilation/constriction is normal, VD in POAG can be explained by chronic vasoconstriction which limits energy supply to retinal (and brain) neurons with subsequent hypo-metabolism (“silent” neurons) or neuronal cell death. We propose that the root cause of POAG is primarily of vascular and not neuronal origin. This understanding can help to better personalize POAG therapy of not only targeting eye pressure but also vasoconstriction to prevent low vision, slowing its progression and supporting recovery and restoration.

Trial registration

ClinicalTrials.gov, # NCT04037384 on July 3, 2019.

中文翻译：

青光眼的血管失调：垂直视野缺损中的视网膜血管收缩和正常的神经血管耦合

目的

青光眼的视力丧失不仅与眼压升高和神经退行性变有关，血管失调（VD）也是一个主要因素。为了优化治疗，需要在更详细地了解 VD 病理学的基础上，更好地理解预测、预防和个性化医学 (3PM) 的概念。具体来说，为了了解青光眼视力丧失的根本原因是否是神经元（变性）或血管起源，我们现在研究了神经血管耦合（NVC）和血管形态及其与青光眼视力丧失的关系。

方法

在原发性开角型青光眼 (POAG) 患者 ( n = 30) 和健康对照 ( n = 22) 中，使用动态血管分析仪对 NVC 进行研究，以量化闪烁光刺激之前、期间和之后的视网膜血管直径，以评估扩张反应神经元激活后。血管特征和扩张与分支水平和视野损伤相关。

结果

与对照组相比，POAG 患者的视网膜动脉和静脉血管直径明显更小。然而，尽管动脉和静脉直径较小，但在神经元激活过程中动脉和静脉扩张均达到正常值。这在很大程度上与视野深度无关，并且因患者而异。

结论

由于扩张/收缩是正常的，POAG 中的 VD 可以通过慢性血管收缩来解释，慢性血管收缩限制了视网膜（和大脑）神经元的能量供应，从而导致代谢低下（“沉默”神经元）或神经元细胞死亡。我们认为 POAG 的根本原因主要是血管来源，而不是神经元来源。这种理解有助于更好地个性化 POAG 治疗，不仅针对眼压，还针对血管收缩，以预防低视力、减缓其进展并支持恢复和恢复。