Ziangirova G G, Antonova O V
Izv Akad Nauk Ser Biol. 1997 Mar-Apr(2):218-23.
We studied cellular aspects of amyloid angiopathy of the iris upon decompensation of ocular pressure and the role of microcirculatory pathology in pathogenesis of the open angle glaucoma. A total of 115 iris biopsies were studied, which were taken during antiglaucoma operations and stained by Congo rot and thioflavine for amyloid and Toluidine blue for glycosaminoglycans. The biopsies from nine patients were studied at the ultrastructural level. Intravasal increase of the concentration of preamyloid proteins during spasms of the arterioles and capillaries should be considered as a provoking moment of the iris amyloidogenesis. Blockade of reticular structures of the microcirculatory basal membranes by preamyloid serum proteins, which provides for shedding of amyloid fibrils, dystrophic changes and detachment of the endothelial cells from the basal membrane, obliteration of lumens of the capillaries and arterioles, disturbed integrity of the microvascular barrier and accumulation of preamyloid and amyloid proteins in the extracellular matrix, ischemia and focal microinfarctions of the iris, and dystrophia of the melanocytes, are subsequent key factors. Amyloid angiopathy of the iris is a cause of ischemia of the anterior eye part, thus creating conditions for increased intraocular pressure and glaucoma.
我们研究了眼压失代偿时虹膜淀粉样血管病的细胞层面情况以及微循环病理在开角型青光眼发病机制中的作用。共研究了115份虹膜活检样本,这些样本取自抗青光眼手术过程中,并用刚果红和硫黄素染色以检测淀粉样蛋白,用甲苯胺蓝染色以检测糖胺聚糖。对9名患者的活检样本进行了超微结构水平的研究。小动脉和毛细血管痉挛期间血管内淀粉样前体蛋白浓度的增加应被视为虹膜淀粉样变发生的激发时刻。淀粉样前体血清蛋白对微循环基底膜网状结构的阻断,导致淀粉样纤维脱落、内皮细胞营养不良性改变和从基底膜脱离、毛细血管和小动脉管腔闭塞、微血管屏障完整性受损以及淀粉样前体蛋白和淀粉样蛋白在细胞外基质中积聚、虹膜缺血和局灶性微梗死以及黑素细胞营养不良,是随后的关键因素。虹膜淀粉样血管病是眼前部缺血的一个原因,从而为眼压升高和青光眼创造了条件。