학술논문

Natural History and Histology in a Rat Model of Laser-Induced Photothrombotic Retinal Vein Occlusion.
Document Type
Article
Source
Current Eye Research. Apr2008, Vol. 33 Issue 4, p365-376. 12p. 4 Black and White Photographs, 2 Charts, 4 Graphs.
Subject
*HISTOLOGY
*LABORATORY rats
*RETINAL diseases
*OPHTHALMOSCOPY
*FLUORESCENCE angiography
*HEMORRHAGE
Language
ISSN
0271-3683
Abstract
Purpose: To observe temporal changes in retinal physiology and histology in a rat model of laser-induced retinal vein occlusion (RVO). Methods: Ophthalmoscopy, fundus photography, and fluorescein angiography (FA) were performed following laser-induced central retinal vein occlusion (CRVO) and branch retinal vein occlusion (BRVO) immediately after laser treatment and at 3 and 6 hr and 2, 4, 7, 14, and 21 days. Retinal histology was examined at 4, 7, 14, and 21 days. Full-field electroretinogram was recorded from both eyes simultaneously at day 4. Results: For CRVO and BRVO, reperfusion of occluded branch veins was observed 1 to 2 days after treatment. Despite complete reperfusion of branch veins, retinal edema and hemorrhages peaked on day 4, and by day 14, treated retinas appeared pale and edematous upon ophthalmoscopy. In BRVO animals, retinal hemorrhages were limited to the vein-occluded region, although edema was more widespread and, to a limited extent, involved the untreated hemi-retina. Significant GCL cell loss was observed in both CRVO and BRVO groups after day 14. Regional analysis showed that relative GCL loss was greatest in the peripheral retina in BRVO group. Electroretinography disclosed moderate to severe functional deficits in photoreceptors, bipolar, and amacrine and ganglion cells. Conclusion: Laser-induced RVO in rats results in targeted vascular occlusion that persisted for 1 to 2 days. Functional deficits were evident and significant GCL cell loss was seen, notably within peripheral retina of the BRVO model. This reproducible model provides a valuable tool for the study of the molecular events associated with retinal ischemia and cell death. [ABSTRACT FROM AUTHOR]