Research has been conducted into vascular abnormalities in the pathogenesis of glaucoma, but conclusions remain controversial. Our aim was to test the hypothesis that retinal endothelial dysfunction induced by elevated intraocular pressure (IOP) persists after IOP normalization, further triggering retinal ganglion cell (RGC) loss. High intraocular pressure (HP) was induced in mice by episcleral vein occlusion (EVO). Retinal vascular function was measured via video microscopy in vitro. The IOP, RGC and their axons survival, levels of oxidative stress and inflammation as well as vascular pericytes coverage, were determined. EVO caused HP for two weeks, which returned to baseline afterwards. Mice with HP exhibited endothelial dysfunction in retinal arterioles, reduced density of RGC and their axons, and loss of pericytes in retinal arterioles. Notably, these values were similar to those of mice with recovered IOP (RP). Levels of oxidative stress and inflammation were increased in HP mice but went back to normal in the RP mice. Our data demonstrate that HP induces persistent endothelial dysfunction in retinal arterioles, which persists one month after RP. Oxidative stress, inflammation, and loss of pericytes appear to be involved in triggering vascular functional deficits. Our data also suggest that retinal endothelial dysfunction does not affect RGC and their axon survival.

中文翻译：

---

眼压引起的视网膜血管内皮功能障碍持续存在，但不会引发视网膜神经节细胞丢失

已经对青光眼发病机制中的血管异常进行了研究，但结论仍然存在争议。我们的目的是验证眼压正常化后由眼压升高（IOP）引起的视网膜内皮功能障碍持续存在的假设，进一步触发视网膜神经节细胞（RGC）损失。通过巩膜外静脉阻塞 (EVO) 在小鼠中诱导高眼压 (HP)。通过体外视频显微镜测量视网膜血管功能。测定了 IOP、RGC 及其轴突存活率、氧化应激和炎症水平以及血管周细胞覆盖率。EVO导致HP两周，之后恢复到基线。HP 小鼠表现出视网膜小动脉内皮功能障碍，RGC 及其轴突密度降低，视网膜小动脉周细胞减少。值得注意的是，这些值与恢复 IOP (RP) 的小鼠的值相似。HP 小鼠的氧化应激和炎症水平增加，但在 RP 小鼠中恢复正常。我们的数据表明，HP 在视网膜小动脉中诱导持续的内皮功能障碍，这种功能在 RP 后持续一个月。氧化应激、炎症和周细胞丢失似乎与触发血管功能缺陷有关。我们的数据还表明视网膜内皮功能障碍不影响 RGC 及其轴突存活。氧化应激、炎症和周细胞丢失似乎与触发血管功能缺陷有关。我们的数据还表明视网膜内皮功能障碍不影响 RGC 及其轴突存活。氧化应激、炎症和周细胞丢失似乎与触发血管功能缺陷有关。我们的数据还表明视网膜内皮功能障碍不影响 RGC 及其轴突存活。