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Lina Daugeliene, Masayuki Niwa, Akira Hara, Hiroyuki Matsuno, Tetsuya Yamamoto, Yoshiaki Kitazawa, Toshihiko Uematsu; Transient Ischemic Injury in the Rat Retina Caused by Thrombotic Occlusion–Thrombolytic Reperfusion. Invest. Ophthalmol. Vis. Sci. 2000;41(9):2743-2747.
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purpose. To establish a clinically relevant model of transient retinal ischemia
by thrombotic occlusion-thrombolytic reperfusion of the central retinal
artery of the rat.
methods. Thrombus was photochemically induced in the central retinal artery by
the combination of intravenous injection of photo-sensitive dye, rose
bengal, and green laser irradiation focused on the artery. Transient
retinal ischemia for 60 minutes was achieved by a subsequent systemic
administration of tissue-type plasminogen activator to reperfuse the
occluded vessel. Samples of retinas were excised from the animals
killed 3, 9, 12, 24, 48, and 78 hours after the reperfusion. The
experimental data were processed using the TdT-dUTP terminal nick-end
labeling (TUNEL) method to detect apoptotic cells.
results. The transient retinal ischemia caused time-sequential apoptotic changes
in the retinal cells as evaluated by counting the number of
TUNEL-positive cells. The most remarkable changes occurred in the
central area of retina, and further on the sections taken 24 hours
after reperfusion. The peripheral area was less affected, and the outer
nuclear cell layer was almost unaffected throughout the observation
conclusions. The proposed method to cause retinal transient ischemia is highly
reproducible, and it is easy to simulate the progress and topographical
distribution of retinal changes observed in the clinical cases of
central retinal arterial occlusion and its subsequent thrombolytic
reperfusion. This may provide a useful tool for constructing the
effective thrombolytic strategies against the central retinal arterial
occlusion and for evaluating the effects of neuroprotective
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