May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
Effect of Chronic Hypoperfusion Secondary to Bilateral Common Carotid Artery Occlusion in Retina of Adult Rats
Author Affiliations & Notes
  • D. Lavinsky
    Department of Biochemistry and department of Ophthalmology and Otorhinolaringology, Federal University of Rio Grande do Sul, Porto Alegre, Brazil
  • N.S. Arteni
    Department of Biochemistry, Federal University of Rio Grande do Sul, Porto Alegre, Brazil
  • M. Achaval Elena
    Department of Morphology, Federal University of Rio Grande do Sul, Porto Alegre, Brazil
  • C.A. Netto
    Department of Morphology, Federal University of Rio Grande do Sul, Porto Alegre, Brazil
  • Footnotes
    Commercial Relationships  D. Lavinsky, None; N.S. Arteni, None; M. Achaval Elena, None; C.A. Netto, None.
  • Footnotes
    Support  PIBIC/CNPq UFRGS
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 4889. doi:
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      D. Lavinsky, N.S. Arteni, M. Achaval Elena, C.A. Netto; Effect of Chronic Hypoperfusion Secondary to Bilateral Common Carotid Artery Occlusion in Retina of Adult Rats . Invest. Ophthalmol. Vis. Sci. 2003;44(13):4889.

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Abstract

Abstract: : Purpose: Bilateral common carotid artery occlusion (BCCAO) of rats results in retinopathy similar to the ocular ischemic syndrome in humans and thus could be used as a model for experimental studies of retinal ischemia. The reduction of blood flow by BCCAO for seven days induces events related to gliosis with increased levels of GFAP, although it does not cause an evident histological damage. Loss of direct photomotor pupillary reflex on the majority of the animals appears in this period. However, after 90 days of BCCAO there is retinal degeneration and cellular death. Our purpose was to investigate the effects of BCCAO for 30 days in retina of adult rats. Methods:Fifteen adults Wistar rats were used, divided in two groups: one submitted to BCCAO and another to sham surgery, in which the arteries were exposed, but not occluded. Both direct and consensual photomotor pupillary reflexes were investigated with a beam of light of an ophthalmoscope before and after the surgery, everyday for the first week and weekly for 30 days. After one month we performed ocular fundus photography ; the animals were perfused with paraformolaldeyde, the eyes were enucleated and fixated in paraffin. Retinal ganglion cell (RGC) density and the thickness of the internal plexiform (IPL), internal nuclear (INL), external plexiform (EPL) and external nuclear layers (ENL) were analyzed. Results:Eight rats were submitted to BCCAO surgery and seven to sham procedure. Half of the BCCAO group lost the direct pupillary reflex in both eyes, three rats lost in one eye and only one maintained in both eyes. In those with unilateral direct pupillary loss, the consensual reflex was preserved. RGC density (cell/mm) was diminished on the left eye of BCCAO group (p<0,05) and there was a significant decrease on the thickness of the IPL in both eyes (p<0,05); however, there were no evident changes on the other layers. Fundus photography did not demonstrate significant difference between BCCAO and sham group. Conclusions:This study demonstrate that BCCAO for 30 days induces functional and morphological damage to the retina with loss of pupillary reflex, decrease on the IPL and cellular death. Therefore this model is suitable for experimental studies on retinal damage induced by reduction of blood flow.

Keywords: ischemia • vascular occlusion/vascular occlusive disease • pupillary reflex 
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