Origin of retinal pigment epithelium cell damage by pulsed laser irradiance in the nanosecond to microsecond time regimen

Citation
R. Brinkmann et al., Origin of retinal pigment epithelium cell damage by pulsed laser irradiance in the nanosecond to microsecond time regimen, LASER SURG, 27(5), 2000, pp. 451-464
Citations number
40
Categorie Soggetti
Surgery
Journal title
LASERS IN SURGERY AND MEDICINE
ISSN journal
01968092 → ACNP
Volume
27
Issue
5
Year of publication
2000
Pages
451 - 464
Database
ISI
SICI code
0196-8092(2000)27:5<451:OORPEC>2.0.ZU;2-R
Abstract
Background and Objective: Selective photodamage of the retinal pigment epit helium (RPE) is a new technique to treat a variety of retinal diseases with out causing adverse effects to surrounding tissues such as the neural retin a including the photoreceptors and the choroid. In this study, the mechanis m of cell damage after laser irradiation was investigated. Study Design/Materials and Methods: Single porcine RPE-melanosomes and RPE cells were irradiated with a Nd:YLF laser (wavelength lambda = 527 nm, adju stable pulse duration tau = 250 nsec-3 mu sec) and a Nd:YAG laser (lambda = 532 nm, tau = 8 nsec). Fast flash photography was applied to observe vapor ization at melanosomes in suspension. A fluorescence viability assay was us ed to probe the cells vitality. Results: The threshold radiant exposures for vaporization around individual melanosomes and for ED50 cell damage are similar at 8-nsec pulse duration. Both thresholds increase with pulse duration; however, the ED50 cell damag e radiant exposure is 40% lower at 3 mu sec. Temperature calculations to mo del the onset of vaporization around the melanosomes are in good agreement with the experimental results when assuming a surface temperature of 150 de greesC to initiate vaporization and a homogeneous melanosome absorption coe fficient of 8,000 cm(-1). Increasing the number of pulses delivered to RPE cells at a repetition rate of 500 Hz, the ED50 value decreases for all puls e durations. However, the behavior does not obey scaling laws such as the N -1/4 equation. Conclusion: The origin of RPE cell damage for single pulse irradiation up t o pulse durations of 3 mu sec can be described by a damage mechanism in whi ch microbubbles around the melanosomes cause a rupture of the cell structur e. The threshold radiant exposure for RPE damage decreases with increasing number of pulses applied. Lasers Surg. Med. 27:451-464, 2000. (C) 2000 Wile y-Liss, Inc.