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青光眼的神经保护——电生理学

Neuroprotection in glaucoma-electrophysiology.

作者信息

Lešták Ján, Fůs Martin

机构信息

Eye Clinic, JL Faculty of Biomedical Engineering CTU in Prague, 158 00 Prague 5, Czech Republic.

CTU in Prague, Faculty of Biomedical Engineering, 272 01 Kladno 2, Czech Republic.

出版信息

Exp Ther Med. 2020 Apr;19(4):2401-2405. doi: 10.3892/etm.2020.8509. Epub 2020 Feb 10.

Abstract

Hypertensive glaucoma is defined as a group of diseases with progressive loss of the neuroretinal margin of the optic disc that causes characteristic degenerative optic neuropathy. The present study provided an updated summary of the physiology and pathology of neurotransmission in the visual path, with the focus on glaucoma. The results of positron emission tomography, functional magnetic resonance imaging and mainly electrophysiological methods demonstrated pathogenesis of nerve cell damage in the visual pathway. Based on these conclusions, neuroprotection in glaucoma was proposed. This consists mainly of the reduction of the intraocular pressure. It is followed by a decrease of glutamate in the synaptic cleft and blockade of its binding to the NMDA receptors. The supply of energy substrates to altered nerve cells is also indispensable. Therapy should be systemic due to impairment of the complete visual path.

摘要

高血压性青光眼被定义为一组疾病,其特征是视盘神经视网膜边缘逐渐丧失,导致典型的退行性视神经病变。本研究提供了视觉通路神经传递生理和病理的最新综述,重点是青光眼。正电子发射断层扫描、功能磁共振成像以及主要的电生理方法的结果证实了视觉通路中神经细胞损伤的发病机制。基于这些结论,提出了青光眼的神经保护措施。这主要包括降低眼压。其次是减少突触间隙中的谷氨酸,并阻断其与NMDA受体的结合。向发生改变的神经细胞供应能量底物也是必不可少的。由于整个视觉通路受损,治疗应是全身性的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60e5/7086198/c6d5eee63ac1/etm-19-04-2401-g00.jpg

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