Algvere P, Jonsson V, Svedbergh B
Albrecht Von Graefes Arch Klin Exp Ophthalmol. 1981;217(4):273-83. doi: 10.1007/BF00429288.
The effects of vitreous hemorrhages on anterior uveal vessels were studied. Albino rabbits were injected intravitreally with autogenous blood, plasma, RBCs, iron-dextrin, or Ringer's solution. The vascular permeability was assessed by fluorescein iris angiography, carbon labeling and penetration of peroxidase. Following one injection of blood, aqueous flare and fluorescein leakage from the iris were observed for 40 days. Intense vascular carbon labeling in iridial and ciliary processes was present for 1-40 days and weak-to-moderate labeling in the iris for 9-40 days. Repeated blood injections aggravated the vascular response, showing extravasation of peroxidase and carbon labeling of iridial vessels for 92 days. The most severe vascular damage ensued from iron-dextrin and RBCs. Plasma an Ringer's solution gave no reaction. The authors suggest that the iron-containing degradation products of RBCs induce vascular damage in anterior uvea and disruption of blood-aqueous barriers.
研究了玻璃体积血对眼前段葡萄膜血管的影响。将白化兔玻璃体腔内注射自体血液、血浆、红细胞、铁-右旋糖酐或林格氏液。通过荧光素虹膜血管造影、碳标记和过氧化物酶渗透评估血管通透性。注射一次血液后，观察到房水闪光和虹膜荧光素渗漏持续40天。虹膜和睫状体出现强烈的血管碳标记持续1 - 40天，虹膜出现弱至中度标记持续9 - 40天。重复注射血液加重了血管反应，显示过氧化物酶外渗和虹膜血管碳标记持续92天。最严重的血管损伤由铁-右旋糖酐和红细胞引起。血浆和林格氏液无反应。作者认为，红细胞含铁血降解产物可导致眼前段葡萄膜血管损伤和血-房水屏障破坏。
