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Treatment of Laser Induced Retinal Injuries
Final rept. 1 Nov 1983-31 Oct 1984
TEL-AVIV UNIV (ISRAEL)
Pagination or Media Count:
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. We have suggested that prostanoids might be involved in laser induced retinal burns and that it is likely that anti-inflammatory drugs which inhibit arachidonic acid metabolism can help accelerate retinal healing. In addition, we have suggested that an increase in prostanoid levels in the retinachoroid or vitreous cavity might cause a break in the blood retinal barriers and protein leakage into the vitreous. Our 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 retinachoroid, and exposed the retina to 30 laser burns. Thus, a single tissue sample was adequate for measurement. Indeed, PGE2 levels in retinachoroid 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 our working model and confirmed our hypothesis of PGE2 and prostacyclin involvement in laser induced retinal damage.
APPROVED FOR PUBLIC RELEASE