Alterations of Ocular Hemodynamics Impair Ophthalmic Vascular and Neuroretinal Function.
Alterations of Ocular Hemodynamics Impair Ophthalmic Vascular and Neuroretinal Function.
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眼部血流动力学的改变会损害眼部血管和神经视网膜功能。
DOI：
10.1016/j.ajpath.2017.11.015
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发表时间：
2018
期刊：
影响因子：
--
通讯作者：
Kuo,Lih
中科院分区：
文献类型：
--
作者：
Tsai,Shu-Huai;Xie,Wankun;Zhao,Min;RosaJr,RobertH;Hein,TravisW;Kuo,Lih
高血压与许多疾病有关，但其对眼循环和神经视网膜功能的直接影响尚不清楚。在此，小鼠眼睛通过横主动脉缩窄受到不同水平的血液动力学损伤的挑战，其在右颈总动脉中分别使血压和流速增加50%和40%，并且在左颈总动脉中分别使这些参数减少30%和40%。在横向主动脉缩窄4周时，右侧视网膜中央动脉的血流速度逐渐增加至40%，左侧视网膜中央动脉的血流速度逐渐降低20%。眼底和视网膜结构未因血流动力学改变而改变。乙酰胆碱和腺苷的内皮依赖性血管舒张仅在右侧（高血压）眼动脉中减少。仅在高血压视网膜中发现神经纤维/神经节细胞层的细胞结构增加、胶质细胞酸性蛋白表达增强和超氧化物水平升高。视网膜电图显示高血压眼暗视b波降低，高血压眼和水肿眼暗视振荡电位降低。总之，持续4周的高血压会导致眼血管功能障碍、视网膜胶质细胞活化、氧化应激和神经视网膜损伤。虽然眼血管调节对水肿不敏感，但眼灌注不足导致神经视网膜功能障碍。
Hypertension is associated with numerous diseases, but its direct impact on the ocular circulation and neuroretinal function remains unclear. Herein, mouse eyes were challenged with different levels of hemodynamic insult via transverse aortic coarctation, which increased blood pressure and flow velocity by 50% and 40%, respectively, in the right common carotid artery, and reduced those parameters by 30% and 40%, respectively, in the left common carotid artery. Blood velocity in the right central retinal artery gradually increased up to 40% at 4 weeks of transverse aortic coarctation, and the velocity in the left central retinal artery gradually decreased by 20%. The fundus and retinal architecture were unaltered by hemodynamic changes. Endothelium-dependent vasodilations to acetylcholine and adenosine were reduced only in right (hypertensive) ophthalmic arteries. Increased cellularity in the nerve fiber/ganglion cell layers, enhanced glial fibrillary acidic protein expression, and elevated superoxide level were found only in hypertensive retinas. The electroretinogram showed decreased scotopic b-waves in the hypertensive eyes and decreased scotopic oscillatory potentials in both hypertensive and hypotensive eyes. In conclusion, hypertension sustained for 4 weeks causes ophthalmic vascular dysfunction, retinal glial cell activation, oxidative stress, and neuroretinal impairment. Although ophthalmic vasoregulation is insensitive to hypotensive insult, the ocular hypoperfusion causes neuroretinal dysfunction.