Kida Teruyo, Flammer Josef, Oku Hidehiro, Konieczka Katarzyna, Morishita Seita, Horie Taeko, Ikeda Tsunehiko
Department of Ophthalmology, Osaka Medical College, Takatsuki, Japan.
Department of Ophthalmology, University of Basel, Basel, Switzerland.
Data Brief. 2018 Sep 29;21:59-62. doi: 10.1016/j.dib.2018.09.070. eCollection 2018 Dec.
Retinal vein occlusion (RVO) is a common vascular disease of the retina; however, the pathogenesis of RVO is still unclear. Branch RVO (BRVO) commonly occurs at the arteriovenous crossing and it was formerly believed that the diseased artery mechanically compresses the vein. However, it has been reported that the retinal vein runs deep beneath the artery at the arteriovenous crossing in eyes with an arterial overcrossing, and the venous lumen often appears to be preserved, even at the arteriovenous crossing, as shown by optical coherence tomography. Paques et al. [1] found venous nicking without arteriovenous contact using adaptive optics imaging. Thus, we investigated the potential role of a dysregulation of the retinal vein. While the pathogenesis of retinal vein occlusion (RVO) is still unclear, systemic hypertension and increased level of endothelin-1 (ET-1) are known risk factors (Flammer and Konieczka, 2015) [2]. We focused on the behavior of retinal veins in spontaneous hypertensive rats (SHR). Then, one of the retinal veins became exceptionally constricted and was nearly occluded (Fig. 1), and the chorioretinal blood flow significantly decreased in the retinas of SHRs following the intravenous injection of ET-1. In addition, immunoreactivity to ET-A receptor was higher in SHR retinas than in control (WKY; Wistar Kyoto rat) retinas (Fig. 2). The protein levels of ET-A receptor and HIF-1 were also significantly higher in SHR retinas than in WKY retinas (Fig. 3). We observed vasoactivity of retinal veins; a retinal venous constriction (Kida et al., 2018) [3]. This supports the hypothesis that ET-1 can constrict retinal veins, thus increasing retinal venous pressure, and that ET-1 may even contribute to the pathogenesis of RVO.
视网膜静脉阻塞（RVO）是一种常见的视网膜血管疾病；然而，RVO的发病机制仍不清楚。分支视网膜静脉阻塞（BRVO）通常发生在动静脉交叉处，以前人们认为患病的动脉会机械性压迫静脉。然而，有报道称，在动脉交叉的眼中，视网膜静脉在动静脉交叉处位于动脉的深部，即使在动静脉交叉处，静脉腔通常似乎也是保留的，这已通过光学相干断层扫描得到证实。帕克等人[1]使用自适应光学成像发现了没有动静脉接触的静脉切迹。因此，我们研究了视网膜静脉调节异常的潜在作用。虽然视网膜静脉阻塞（RVO）的发病机制仍不清楚，但系统性高血压和内皮素-1（ET-1）水平升高是已知的危险因素（弗拉默和科涅茨卡，2015年）[2]。我们关注自发性高血压大鼠（SHR）视网膜静脉的行为。然后，其中一条视网膜静脉异常收缩并几乎闭塞（图1），静脉注射ET-1后，SHR视网膜的脉络膜视网膜血流量显著降低。此外，SHR视网膜中ET-A受体的免疫反应性高于对照组（WKY；Wistar Kyoto大鼠）视网膜（图2）。SHR视网膜中ET-A受体和HIF-1的蛋白水平也显著高于WKY视网膜（图3）。我们观察到了视网膜静脉的血管活性；视网膜静脉收缩（木田等人，2018年）[3]。这支持了以下假设：ET-1可使视网膜静脉收缩，从而增加视网膜静脉压，并且ET-1甚至可能促成RVO的发病机制。
