Background:Stroke-related loss of vision is one of the residual impairments, restricting the quality of life. However, studies of the ocular manifestations of asphyxia cardiac arrest/resuscitation (ACA/R) have reported very heterogeneous results. Objective:We aimed to evaluate the ACA/R-induced degeneration pattern of the different retinal cell populations in rats using different immuno-histological stainings. Methods:The staining pattern of toluidine blue and the ganglion cell markers β-III-tubulin and NeuN; the calcium-binding protein parvalbumin, indicating ganglion, amacrine, and horizontal cells; calretinin D28k, indicating ganglion and amacrine cells; calbindin, indicating horizontal cells; Chx 10, indicating cone bipolar cells; PKCα, indicating ON-type rod bipolar cells; arrestin, indicating cones; and rhodopsin, a marker of rods, as well as the glial cell markers GFAP (indicating astroglia and Müller cells) and IBA1 (indicating microglia), were evaluated after survival times of 7 and 21 days in an ACA/R rat model. Moreover, quantitative morphological analysis of the optic nerve was performed. The ACA/R specimens were compared with those from sham-operated and completely naïve rats. Results:ACA/R-induced effects were: (i) a significant reduction of retinal thickness after long-term survival; (ii) ganglion cell degeneration, including their fiber network in the inner plexiform layer; (iii) degeneration of amacrine and cone bipolar cells; (iv) degeneration of cone photoreceptors; (v) enhanced resistance to ACA/R by rod photoreceptors, ON-type rod bipolar and horizontal cells, possibly caused by the strong upregulation of the calcium-binding proteins calretinin, parvalbumin, and calbindin, counteracting the detrimental calcium overload; (vi) significant activation of Müller cells as further element of retinal anti-stress self-defense mechanisms; and (vii) morphological alterations of the optic nerve in form of deformed fibers. Conclusions:Regardless of the many defects, the surviving neuronal structures seemed to be able to maintain retinal functionality, which can be additionally improved by regenerative processes true to the “use it or lose it” dogma.

中文翻译：

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窒息致短暂性心脏骤停后大鼠视网膜抗性柱状单元和易损网络的免疫组织学检测

背景：中风相关的视力丧失是一种残余损伤，限制了生活质量。然而，对窒息性心脏骤停/复苏 (ACA/R) 的眼部表现的研究报告了非常不同的结果。目的：我们旨在使用不同的免疫组织学染色评估 ACA/R 诱导的大鼠不同视网膜细胞群的变性模式。方法：甲苯胺蓝染色模式及神经节细胞标志物β-III-微管蛋白和NeuN；钙结合蛋白小白蛋白，指示神经节、无长突和水平细胞；钙调蛋白 D28k，指示神经节和无长突细胞；钙结合蛋白，表示水平细胞；Chx 10，表示锥形双极细胞；PKCα，表示ON型杆状双极细胞；抑制素，指示锥体；和视紫红质，一种视杆标记物，以及胶质细胞标志物 GFAP（表示星形胶质细胞和 Müller 细胞）和 IBA1（表示小胶质细胞），在 ACA/R 大鼠模型中存活 7 天和 21 天后进行了评估。此外，还进行了视神经的定量形态学分析。将 ACA/R 标本与来自假手术和完全幼稚大鼠的标本进行比较。结果：ACA/R 诱导的效果是：（i）长期存活后视网膜厚度显着减少；(ii) 神经节细胞变性，包括它们在内丛状层中的纤维网络；(iii) 无长突细胞和锥双极细胞的退化；(iv) 视锥细胞退化；(v) 杆状光感受器、ON 型杆状双极细胞和水平细胞对 ACA/R 的抗性增强，这可能是由钙结合蛋白钙调蛋白、小白蛋白的强烈上调引起的，和钙结合蛋白，抵消有害的钙超载；(vi) Müller 细胞的显着激活作为视网膜抗应激自卫机制的进一步元素；(vii) 变形纤维形式的视神经形态学改变。结论：尽管存在许多缺陷，幸存的神经元结构似乎能够维持视网膜功能，这可以通过忠实于“使用它或失去它”教条的再生过程得到额外改善。