April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Longitudinal Evaluation of Spontaneous Haemorrhages in the Rat Retina and AMD-like Lesions
Author Affiliations & Notes
  • Nigel L. Barnett
    Centre for Clinical Research, University of Queensland, Brisbane, Australia
  • Matthew J. Brazel
    Centre for Clinical Research, University of Queensland, Brisbane, Australia
  • David V. Pow
    Centre for Clinical Research, University of Queensland, Brisbane, Australia
  • Footnotes
    Commercial Relationships  Nigel L. Barnett, None; Matthew J. Brazel, None; David V. Pow, None
  • Footnotes
    Support  NHMRC (Australia)
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 940. doi:
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    • Get Citation

      Nigel L. Barnett, Matthew J. Brazel, David V. Pow; Longitudinal Evaluation of Spontaneous Haemorrhages in the Rat Retina and AMD-like Lesions. Invest. Ophthalmol. Vis. Sci. 2011;52(14):940.

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

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Abstract
 
Purpose:
 

To evaluate the long-term consequences of retinal haemorrhage in the young pigmented rat.

 
Methods:
 

A spontaneous model of retinal haemorrhage which was discovered in this laboratory was evaluated longitudinally by means of fundus photography. Final pathology was evaluated histologically and by immunocytochemistry.

 
Results:
 

We demonstrate bleeding in the eyes of all rats examined (n=95). Fundus photographs (see image) revealed that bleeding commenced at around 2 weeks of age and active bleeding appeared to cease at around 6 weeks of age. Cells of the monocyte lineage including macrophages were subsequently observed at the sites of bleeding, and haemosiderin-containing macrophages persisted for at least 12 months at such sites. Photoreceptor degeneration was observed at approximately 9 months post-haemorrhage, with subsequent anomalies in vascularization and glial cell reactivity.

 
Conclusions:
 

Haemorrhage in the retina leads to a slow degenerative phenotype with features that are comparable to aspects of AMD. We suggest that activation of the clotting cascade, which co-activates the complement cascade, may be an initiating factor in the degenerative process in this model, and possibly in human AMD.  

 
Keywords: blood supply • degenerations/dystrophies • microglia 
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