Elucidation of the dysfunctional mechanisms of retinal circulation in the rat models of glaucoma and exploration of novel therapeutic drugs for glaucoma.

在视网膜缺血-再灌流或玻璃体内注射N-甲基-D-天冬氨酸诱导的青光眼大鼠模型中，视网膜血管的血管扩张反应通过激活内皮细胞的机制而不是对平滑肌的直接刺激而被减弱。这些结果提示，青光眼视网膜循环异常可能加速了视网膜的退变。提示在缺血再灌流模型中，内皮素-1在引起视网膜血管严重收缩中起重要作用。前列腺素EP2受体拮抗剂能扩张青光眼模型大鼠视网膜血管，与正常大鼠一样，抑制视网膜神经损伤。这些结果提示前列腺素EP2受体激动剂可能是预防和/或治疗青光眼的新候选药物。

I revealed that vasodilator responsesof retinal blood vesselsmediated through the mechanism via activation ofendothelial cells, but not those to direct stimulation of smooth muscle, was attenuated in the rat models of glaucoma, which was inducedby retinal ischemia-reperfusionorintravitreal injection of N-methyl-D-aspartic acid. These results suggested that abrormal retinal circulation in glaucoma may accelerateretinal degeneration. It was also suggested that endothelin-1 played an important role to induce severe constriction of theretinal vasculature in the ischemia-reperfusion model. Anagonist of prostanoid EP2 receptor dilatedretinal bloodvessels in the glaucoma model rats, as in the normal rats and inhibited the retinal nerve injury. These results suggestthat prostanoid EP2 receptor agonistsmay be novel candidate drugsfor prevention and/or treatment of glaucoma.