May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Dynamics of Structural Changes of Laser–Induced Retinal Injury in Rats
Author Affiliations & Notes
  • M. Belokopytov
    Goldschleger Eye Res Institute, Tel Aviv University, Tel Hashomer, Israel
  • G. Dubinsky
    Goldschleger Eye Res Institute, Tel Aviv University, Tel Hashomer, Israel
  • Y. Epstein
    Goldschleger Eye Res Institute, Tel Aviv University, Tel Hashomer, Israel
  • M. Belkin
    Goldschleger Eye Res Institute, Tel Aviv University, Tel Hashomer, Israel
  • M. Rosner
    Goldschleger Eye Res Institute, Tel Aviv University, Tel Hashomer, Israel
  • Footnotes
    Commercial Relationships  M. Belokopytov, None; G. Dubinsky, None; Y. Epstein, None; M. Belkin, None; M. Rosner, None.
  • Footnotes
    Support  MOD, Israel
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 155. doi:
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    • Get Citation

      M. Belokopytov, G. Dubinsky, Y. Epstein, M. Belkin, M. Rosner; Dynamics of Structural Changes of Laser–Induced Retinal Injury in Rats . Invest. Ophthalmol. Vis. Sci. 2005;46(13):155.

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

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Abstract

Abstract: : Purpose: Retinal photocoagulation lesions undergo primary and secondary degeneration followed by partial repair. This study follows the temporal changes in laser–induced retinal lesion. Methods: Standard lesions were created by argon laser (514 & 544 nm, 200 mm, 0.1 W, 0.05 second) in 36 DA pigmented rats. Sections of the retinal lesions were evaluated by light microscopy 1, 24, 48, 72 hours, and 20, and 60 days after the primary injury (six animals at each time point). Results: The diameter of the lesion was equal to that of the laser spot 1h after irradiation and increased by 24h due to serous edema around the lesion in RPE. The edema decreased slightly during the following 48h and significantly by 20 days. One hour after photocoagulation inner and outer segment were edematous, with loss of structure and disappearance of the border between inner and outer layers, and between photoreceptors. The destruction of photoreceptors (complete loss of discrimination between the segments) was most severe after 24–48h. The nuclei in the outer–nuclear layer were pyknotic at the lesion site at 1h and disappeared later. Healing processes began 72h after the irradiation and was completed by 60 days. Filling–in by sliding of near nuclei was observed by the 60th day. Reversible changes were seen also in the retinal pigment epithelium (with formation of a plaque, composed of proliferating retinal pigment epithelium, macrophages, capillaries and dispersed pigment granules, at 72h and its degradation later on) and in the choroid (disorganization of capillaries by 48h with later reorganization). Conclusions: The development of a laser–induced injury is gradual. The photoreceptors are damaged first and than the damage spreads to other layers of retina and to areas neighboring the primary injury site. The secondary degeneration is accompanied by an inflammatory process. The extension of the damage is later stopped and the adjacent tissues tend to fill the lesion and remodel the retina.

Keywords: laser • photoreceptors • wound healing 
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