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U.S. Department of Energy
Office of Scientific and Technical Information

Treatment of laser-induced retinal injuries. Final report, 1 November 1983-31 October 1984

Technical Report ·
OSTI ID:6676467
Prostanoids are mediators of the inflammatory process in many organs, including the eye, and their production from arachidonic acid is triggered by a variety of stimuli including laser burns. The authors have suggested that prostanoids might be involved in laser induced retinal burns and that it is likely that anti-inflammatory drugs that inhibit arachidonic acid metabolism can help accelerate retinal healing. In addition, they have suggested that an increase in prostanoid levels in the retina/choroid or vitreous cavity might cause a break in the blood retinal barriers and protein leakage into the vitreous. Their preliminary study indicates that both a single retinal laser burn and 10 laser burns cause an increase in PGE2 and prostacyclin levels of the choroid at 18 hours after lasing. However, results were inconsistent and required the use of 3 samples of each tissue for a single determination. Modifications done in order to overcome these problems involved the use of a tissue preparation of unseparated retina/choroid, and exposed the retina to 30 laser burns. Thus, a single tissue sample was adequate for measurement. Indeed, PGE2 levels in retina/choroid and vitreous of eyes subjected to 30 moderate laser applications demonstrated an increase in prostaglandin E2 (PGE2) and prostacyclin levels throughout a 3-day period after lasing. This mode of lasing was chosen as the working model and confirmed the hypothesis of PGE2 and prostacyclin involvement in laser induced retinal damage.
Research Organization:
Tel Aviv Univ. (Israel)
OSTI ID:
6676467
Report Number(s):
AD-A-196486/5/XAB
Country of Publication:
United States
Language:
English