ObjectiveTo observe the concentration of plasma endothelin (ET-1) in patients with nonarteritic anterior ischemic optic neuropathy(NAION) and investigate the relationship between ET-1 and NAION.MethodsThe plasma levels of ET-1 in 41 patients with NAION and 15 age-matched normal control subjects were measured by radioimmuoassay (RIA). The patients with NAION were divided into high papilloedema group, light papilloedema group, and recovery group according to the degree of papilloedema; and were divided into group1 (within 14 days), 2 (within 15-30 days), 3 (within 31-60 days), and 4 (within 61-180 days) according to the disease course. The plasma levels of ET-1 in different groups were detected and compared.ResultsThe plasma level of ET-1 in patients with NAION was significantly higher than that in the normal subjects (t=5.02，P＜0.05）and there was no obvious difference in NAION patients with different genders.There were significant differences of the plasma level among the groups with different degree of papilloedema（F=4.65，P＜0.05）. ET-1 plasma level gradually decreased as the disease course increased, and there were significant differences among the groups with different disease course（F=4.29，P＜0.05）. The difference of plasma level of ET-1 between Group 13 with corresponding disease courses and the control group was significant respectively(t1=5.92，t2=3.47，t3=2.18， P1lt;0.01, P2lt;0.05, P3lt;0.05)ConclusionThe plasma level of ET-1 in patients with NAION may be related to the degree of papilloedema lesion and disease courses. (Chin J Ocul Fundus Dis, 2005,21:156-158)
Ras homolog family (Rho)/ Rho-associated coiled-coil kinase (ROCK) signaling pathway widely exists in human and mammal cells, which is closely related to inhibition of repair after optic nerve damage. The expression level of Rho/ROCK signaling pathway-related proteins is up-regulated in glaucoma, and related with the death of retinal ganglionic cell (RGC) and the axon activity. ROCK inhibitors can protect the surviving RGC and promote axon extension with a dose-dependent manner. ROCK inhibitors also can inhibit glial scar formation, lower intraocular pressure and inhibit inflammatory response to some degrees. Rho/ROCK signaling pathway correlates with the optic nerve disease progression, and ROCK inhibitors hope to become a new therapeutic drug.