Ischemia-reperfusion causes exudative detachment of the rabbit retina.
Ischemia-reperfusion causes exudative detachment of the rabbit retina.
复制标题
缺血再灌注导致兔视网膜渗出性脱离。
DOI：
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发表时间：
2005
影响因子：
4.4
通讯作者：
A. Bringmann
中科院分区：
文献类型：
--
作者：
Ortrud Uckermann;S. Uhlmann;T. Pannicke;M. Francke;Ruslan Gamsalijew;F. Makarov;Elke Ulbricht;P. Wiedemann;A. Reichenbach;N. Osborne;A. Bringmann
目的
研究兔视网膜缺血-再灌注过程中大胶质细胞（Müller）和小胶质细胞的活化以及神经元细胞变性，并检测曲安奈德对胶质增生的可能影响。
方法
通过增加眼内压60分钟来产生暂时性视网膜缺血。在缺血停止后立即玻璃体内应用曲安奈德（8 mg）。在再灌注后第3天和第8天，记录急性分离的Müller细胞的K+电流，并在视网膜整体上用荧光法记录Müller细胞对P2Y受体刺激的Ca 2+反应。用isolectin标记视网膜整体的神经纤维层中的小胶质细胞/免疫细胞。为了评估神经元和Müller细胞损失，在视网膜切片中计数细胞数量。
结果
短暂性缺血引起中央视网膜的渗出性脱离，其特征在于色素上皮单层的破坏，在扩展的视网膜下腔中存在分散的色素上皮和免疫细胞，以及视网膜褶皱。再灌注后8天，观察到感光细胞的显著损失。再灌注后3天和8天，Müller细胞胶质增生明显，表现为细胞肥大、K+通道表达下调和显示P2Y受体介导的Ca 2+反应的细胞数量增加。再灌注后小胶质细胞/免疫细胞的数量强烈增加。玻璃体内注射曲安奈德不影响Müller细胞胶质增生的参数，但减少了小胶质细胞/免疫细胞的数量。
结论
兔视网膜缺血再灌注引起渗出性视网膜脱离，其特征在于感光细胞的损失，而内层视网膜大部分保留。微胶质细胞和大胶质细胞在再灌注早期被激活，甚至在感光细胞脱落之前。玻璃体内注射曲安西龙可能会降低小胶质细胞/免疫细胞活化的程度。
PURPOSE
To characterize the activation of macroglial (Müller) and microglial cells, as well as neuronal cell degeneration, during ischemia-reperfusion in rabbit retina and to test the possible effect of triamcinolone acetonide on gliosis.
METHODS
Transient retinal ischemia was produced by increasing intraocular pressure for 60 minutes. Triamcinolone (8 mg) was intravitreally applied immediately after the cessation of ischemia. At 3 and 8 days after reperfusion, the K+ currents of acutely isolated Müller cells were recorded, and the Ca2+ responses of Müller cells on stimulation of P2Y receptors were recorded fluorometrically in retinal wholemounts. Microglial/immune cells in the nerve fiber layer of retinal wholemounts were labeled with isolectin. To evaluate neuronal and Müller cell loss, the numbers of cells were counted in retinal slices.
RESULTS
Transient ischemia caused exudative detachment of the central retina that was characterized by disruption of the pigment epithelial monolayer, the presence of scattered pigment epithelial and immune cells in the expanded subretinal space, and retinal folds. A significant loss of photoreceptor cells was observed at 8 days after reperfusion. At 3 and 8 days after reperfusion, Müller cell gliosis was apparent, as indicated by cellular hypertrophy, downregulation of K+ channel expression, and an increased number of cells that displayed P2Y receptor-mediated Ca2+ responses. The number of microglial/immune cells increased strongly after reperfusion. Intravitreal triamcinolone did not affect the parameters of Müller cell gliosis but decreased the number of microglial/immune cells.
CONCLUSIONS
Ischemia-reperfusion of the rabbit retina causes exudative retinal detachment that is characterized by a loss of photoreceptor cells, whereas the inner retina remains largely preserved. Micro- and macroglial cells are activated early during reperfusion, even before dropout of the photoreceptor cells. Intravitreal triamcinolone may decrease the degree of microglial/immune cell activation.
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影响因子：
4.4
作者：
D. Rosenbaum;P. Rosenbaum;H. Gupta;Manjeet Singh;A. Aggarwal;D. Hall;S. Roth;J. Kessler
通讯作者：
D. Rosenbaum;P. Rosenbaum;H. Gupta;Manjeet Singh;A. Aggarwal;D. Hall;S. Roth;J. Kessler
缺血再灌注损伤后大鼠视网膜蛋白酪氨酸磷酸化增加。
DOI：
--
发表时间：
1996
期刊：
Investigative ophthalmology & visual science.
影响因子：
--
作者：
Hayashi,A;Koroma,BM;Imai,K;deJuanJr,E
通讯作者：
deJuanJr,E
外视网膜缺血性梗塞——一种新认识的白内障摘除术和闭合性玻璃体切除术的并发症。
影响因子：
13.7
作者：
Parrish,R;Gass,JD;Anderson,DR
通讯作者：
Anderson,DR
DOI：
--
发表时间：
2000
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
G. Tezel;M. Wax
通讯作者：
G. Tezel;M. Wax
影响因子：
4.4
作者：
Keith R G Martin;H. Levkovitch-Verbin;Danielle F Valenta;Lisa A. Baumrind;M. Pease;H. A. Quigley
通讯作者：
Keith R G Martin;H. Levkovitch-Verbin;Danielle F Valenta;Lisa A. Baumrind;M. Pease;H. A. Quigley