May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Natural History of Experimental Branch Retinal Vein Occlusion in Rodents
Author Affiliations & Notes
  • M. Paques
    U 592, Laboratoire de Physiopathologie cellulaire et moléculaire de la rétine, Paris, France
    Institut de la Vision, Université Paris VI, Hôpital Saint–Antoine, Paris, France
  • M. Simonutti
    U 592, Laboratoire de Physiopathologie cellulaire et moléculaire de la rétine, Paris, France
    Institut de la Vision, Université Paris VI, Hôpital Saint–Antoine, Paris, France
  • E. Levavasseur
    U 482, Paris, France
  • J.–A. Sahel
    U 592, Laboratoire de Physiopathologie cellulaire et moléculaire de la rétine, Paris, France
    Institut de la Vision, Université Paris VI, Hôpital Saint–Antoine, Paris, France
  • Footnotes
    Commercial Relationships  M. Paques, hoescht marion roussel F; M. Simonutti, None; E. Levavasseur, None; J. Sahel, None.
  • Footnotes
    Support  Hoescht Marion Roussel
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 4057. doi:
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    • Get Citation

      M. Paques, M. Simonutti, E. Levavasseur, J.–A. Sahel; Natural History of Experimental Branch Retinal Vein Occlusion in Rodents . Invest. Ophthalmol. Vis. Sci. 2005;46(13):4057.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: To detail the natural history of transient branch retinal vein occlusion (BRVO) in rodents. Methods: One or two BRVO was induced by laser photocoagulation in pigmented and albino rodents, and in transgenic CX3CR1 mice expressing gfp in microglial cells. Repeated confocal scanning laser ophthalmoscopy imaging was correlated to histology. Results: Within hours after BRVO induction, rupture of the blood–retinal barrier in the outer microvessel layer, infiltration by activated microglial cells, ICG staining of venous wall, retinal detachment and extensive venous collateralization were evidenced by cSLO and confirmed by histology. In the following weeks, despite recanalization of the occluded vein, persistent collateral circulation was observed, as well as alteration of fundus autofluorescence. The latter was correlated to the extent of retinal damage. Limited retinal damage in the one vein model (loss of the outer plexiform layer) contrasted with the extensive retinal atrophy observed in the two veins model. Retinal atrophy predominated in the outer retina, with significant variations between animals. No new vessels developed. Light deprivation had no effect on retinal atrophy. Variations between species and strains were noted, albino mice having the most prolonged duration of occlusion and the most rapid development of collateral vessels. Conclusions: cSLO complements histology for evaluation of experimental BRVO, especially for the analysis of vascular anatomy, of fundus autofluorescence, and of gfp–expressing cells. BRVO in rodents is a convenient, adjustable and clinically relevant model for the study of neuroprotective strategies.

Keywords: vascular occlusion/vascular occlusive disease • imaging methods (CT, FA, ICG, MRI, OCT, RTA, SLO, ultrasound) • ischemia 
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