Repair of the Pigment Epithelial Barrier Following Photocoagulation

Wallow, Ingolf H. L.

doi:10.1001/archopht.1984.01040030104047

Cited by 114 publications

(46 citation statements)

References 6 publications

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“…Laser photocoagulation may disrupt the outer blood-retina barrier with diffusion of metabolites stimulating endothelial repair and recovery of the inner blood-retina barrier [17]. On the other hand, grid photocoagulation may improve the function of retinal pigment epithelial cells which are responsible for the outer retina-blood barrier [13]. Finally, the coagulative necrosis of the pigment epithelium produces a factor promoting the restoration of the blood-retina barrier [17].…”

Section: Discussionsupporting

confidence: 39%

“…Our understanding of the mechanisms responsible for the breakdown of the blood-retina barrier and the development of macular edema in diabetics has increased in recent years. The loss of the barrier function can be explained by damage of the retinal endothelial junctions [13]. Although diabetic macular edema can spontaneously resolve [16], the ETDRS has demonstrated the value of laser treatment in preventing or reversing visual loss from diabetic macular edema [12].…”

Section: Discussioncontrasting

confidence: 39%

“…The Early Treatment of Diabetic Retinopathy Study (ETDRS) showed the benefit of focal or grid photocoagulation in clinically significant macular edema [12]. The exact mechanism of the grid photocoagulation is unknown, but there is experimental evidence that the blood-retina barrier is restored after treatment [13]. …”

Section: Introductionsupporting

confidence: 39%

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Aqueous Flare and Macular Edema in Eyes with Diabetic Retinopathy

2003

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Background: The breakdown of the blood-retina barrier in diabetic patients is correlated with a dysfunction of the blood-aqueous barrier. In our study, we wanted to investigate the effect of grid photocoagulation in diabetic macular edema on the aqueous flare. Methods: Modified grid pattern photocoagulation was performed on 20 patients with diabetic macular edema. The aqueous flare intensity was measured by the laser flare cell meter before and 4 months after laser treatment. Results: The mean flare value was 9.8 ± 4.7 photons/ms before laser treatment. After grid photocoagulation, the flare value was 7.1 ± 3.6 photons/ms. Flare values were significantly decreased after laser treatment. Conclusion: Our results suggest a correlation between the effect of grid photocoagulation on the blood-retina barrier and the permeability of the blood-aqueous barrier. The laser flare intensity seems to be a quantitative indicator for the diabetic dysfunction of the blood-retina barrier.

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Section: Discussionsupporting

confidence: 39%

Section: Discussioncontrasting

confidence: 39%

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Aqueous Flare and Macular Edema in Eyes with Diabetic Retinopathy

2003

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“…In clinical retinal photocoagulation, for example, with exposure times of several hundred milliseconds, the nonabsorbing neural retina is thermally damaged because it is directly adjacent to the absorbing retinal pigment epithelium (RPE). However, in several diseases only the destruction of the RPE, a single cell layer, is required (3)(4)(5).…”

mentioning

confidence: 46%

Microphotocoagulation: selective effects of repetitive short laser pulses.

Roider

Hillenkamp

Flotte

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

209

150

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Repetitive exposure to short laser pulses is shown to cause seective damage to absorbing structures (cells, organles, or enzymes) with pulse energies below the treshold energy for single-pulse damag. Detly adjacent strucures are spared in Wvo. Additvity of (presummbly nonphotochemical) (1,2). Depending on the exposure time, these effects may not be confined to the absorbing structures. During and after exposure, heat dissipates out of the absorbing volume, causing a substantial temperature increase in the surrounding tissue and undesirable side effects. In clinical retinal photocoagulation, for example, with exposure times of several hundred milliseconds, the nonabsorbing neural retina is thermally damaged because it is directly adjacent to the absorbing retinal pigment epithelium (RPE). However, in several diseases only the destruction of the RPE, a single cell layer, is required (3-5).Such confined effects require the use ofpulses shorter than the thermal relaxation time of the target structure (adiabatic heating) (6). Thermal effects are temperature-and timedependent and highly nonlinear (1, 6-8). As the exposure time and therefore the time of increased temperature becomes shorter, higher temperatures are necessary to achieve a given effect. If the energy is deposited in a very short time (typically microseconds or less), large spatial and temporal temperature gradients result, inducing mechanical effects such as microexplosions, displacement of absorbing structures (e.g., melanin granules), or hemorrhage (9-12). Such gross mechanical effects are often not tolerable in clinical applications. This paper discusses the concept of inducing tissue damage by repetitive short subthreshold pulses, each too small in energy to cause tissue damage by itself, in order to circumvent this limitation.Additivity has been demonstrated for multiple 40-p,s pulses at 488 nm and 647 nm on the retina (13) and for multiple 9-ms CO2 laser pulses on the cornea (14).As an experimental model for such a selective damage mechanism, the rabbit retina has been chosen. The goal of this study was to destroy selectively the RPE cell monolayer by using multiple subthreshold effects with minimal damage to the directly adjacent photoreceptors in the neural retina.The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact. ConceptThe transition from localized to more widespread thermal damage occurs as the exposure duration exceeds the thermal relaxation time (tr) of the target structure. For a thermal point source tr = r2/6k, where k is the thermal diffusivity (1.5 x 10-3 cm2-s-1 for water) (1, 15). tr is defined as the time at which the temperature at a point at distance r from the source has its maximum temperature. During exposure to long pulses (p >> tr), heat transfer occurs and the adjacent tissue is heated relatively uniformly, causing nonspecific necrosis.If the pulse duratio...

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“…6 The laser affected areas of the photoreceptor outer segments and RPE exhibit signs of necrosis including cell disruption, vacuolisation, and condensation of cytoplasmic proteins within a few hours after treatment 4 to an extent that is commensurate with the intensity of the burn. 5 Within days, RPE cells migrate across Bruch's membrane to fill the lesion with subsequent scar formation. 8 9 Müller cells and astrocytes replace the damaged outer nuclear layer of the retina, interdigitating with the migrated RPE cells.…”

mentioning

confidence: 99%

Conditioned medium from mixed retinal pigmented epithelium and Muller cell cultures reduces in vitro permeability of retinal vascular endothelial cells

Tretiach¹

2004

British Journal of Ophthalmology

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Aim: To investigate the in vitro effect of laser photocoagulation on blood-retinal barrier permeability. Methods: Retinal capillary endothelial cells were exposed to supernatants from long term co-cultured cells that were argon laser treated. Endothelial cell permeability was analysed by (1) measurement of transendothelial electrical resistance and (2) Results: Laser photocoagulation of various retinal cells and control ECV304 cells in the lower chamber did not appreciably improve permeability of the endothelial cell monolayer compared with that of unlasered cells. However, medium that was conditioned by mixed retinal pigmented epithelium and Müller cells significantly reduced both inulin (43.2% (SD 6.5%) equilibration in mixed cultures v 59.8% (SD 7.0%) control cells, p,0.05) and albumin (15.1% (SD 3.8%) v 31.1% (SD 6.7%), p,0.05) permeability of the endothelial cell monolayers. A fourfold increase in transendothelial electrical resistance was also seen. Conclusions: These results are consistent with the hypothesis that interaction of Müller cells with retinal pigmented epithelium induced by laser treatment results in secretion of soluble factor(s), which reduces permeability of retinal vascular endothelium. Identification of these factor(s) may have implications for the clinical treatment of macular oedema secondary to diabetic retinopathy and other diseases.

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Repair of the Pigment Epithelial Barrier Following Photocoagulation

Cited by 114 publications

References 6 publications

Aqueous Flare and Macular Edema in Eyes with Diabetic Retinopathy

Aqueous Flare and Macular Edema in Eyes with Diabetic Retinopathy

Microphotocoagulation: selective effects of repetitive short laser pulses.

Conditioned medium from mixed retinal pigmented epithelium and Muller cell cultures reduces in vitro permeability of retinal vascular endothelial cells

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