Terelak-Borys Barbara
Z Kliniki Okulistyki Centrum Medycznego Kształcenia Podyplomowego SPSK im. prof. W. Orlowskiego w Warszawie.
Klin Oczna. 2005;107(4-6):306-11.
Vasospasm in the vessels, supporting the optic disc, is nowadays considered one of the possible etiological factors leading to development of glaucomatous neuropathy. This article describes physiological regulatory mechanisms of blood circulation in these vessels, including influence of autonomic nervous system and blood flow autoregulation; it also explains why vasospasm may disturb autoregulation. Special attention is paid to the role of vascular endothelial mediators, which are responsible for autoregulation. Observations indicating that vasospasm may be a risk factor of glaucomatous damage are also presented. The article describes data concerning vasospastic effects of two mediators: endothelin-1 (ET-1), released by vascular endothelium, and neuropeptide Y (NPY), a sympathetic nervous system neurotransmitter, on the vessels supporting the optic disc and their possible role in producing blood flow disturbances in these vessels. Investigation results indicating that endothelial dysfunction, connected with increased ET-1 plasma levels and sympathetic nervous system disorders, may be involved in the pathogenesis of normal-tension glaucoma, are presented.
如今，支持视盘的血管痉挛被认为是导致青光眼性神经病变发展的可能病因之一。本文描述了这些血管中血液循环的生理调节机制，包括自主神经系统的影响和血流自动调节；还解释了血管痉挛为何会干扰自动调节。特别关注了负责自动调节的血管内皮介质的作用。还介绍了表明血管痉挛可能是青光眼性损害危险因素的观察结果。本文描述了两种介质的血管痉挛效应的数据：血管内皮释放的内皮素 -1（ET -1）和交感神经系统神经递质神经肽 Y（NPY）对视盘支持血管的作用及其在这些血管中产生血流紊乱的可能作用。还介绍了研究结果，表明与血浆 ET -1 水平升高和交感神经系统紊乱相关的内皮功能障碍可能参与正常眼压性青光眼的发病机制。
