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Supplemental oxygen after detachment may save retinal cells, experiments find
Two animal studies suggest that the technique may be clinically valuable.
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SANTA BARBARA, Calif. — Two experimental studies of cats with laboratory-induced retinal detachments found that retinal cell death can be minimized if subjects receive high doses of supplemental oxygen after the detachment, but prior to surgical repair.
Following a retinal detachment, the outer retina is separated from the choroid and thereby deprived of essential oxygen and nutrients, usually compounding damage. In an oxygen-rich environment, cells are less starved, so less damage occurs. Though conducted in cats, the study is likely applicable to human patients with retinal detachment as well, scientists say.
More vulnerable
Oxygen supplementation may prove essential following retinal detachment because retinal cells seem to be more vulnerable to rapid apoptosis. They tend to consume nutrients faster and in greater quantity than similar cells, meaning that within a short period of time after injury, significant damage has already taken place.
The concentration of death and degeneration in the photoreceptors of the detached retina can be explained by the pattern of nutrient supply to the retina. The inner layers are supplied by the retinal circulation, which are unaffected by detachment. The outer layer, comprising the photoreceptors, is supplied by diffusion from the choriocapillaris. Detachment separates the photoreceptors from their only source of the two molecules essential for their metabolism: oxygen and glucose. Analysis of the metabolism of photoreceptors has shown that their metabolic rate is higher than that of other neurons, which, scientists speculate, may heighten their vulnerability to detachment.
Oxygen mitigates damage
To assess the role of hypoxia in causing the death and deconstruction of photoreceptors in detached retinas and the effectiveness of supplemental oxygen in limiting the damage, the U.S. team and an Australian group at the University of Sydney, induced retinal detachment in the right eyes of 10 cats.
Following the induced detachment, the animals were placed in Plexiglass chambers. Two cats were kept in a normal oxygen environment, where the relative oxygen level was 21%. The eight other cats were kept in a hyperoxic environment of 70% oxygen. Reparative surgery was not performed and the eyes were assessed 72 hours after surgery.
Earlier work of the U.S. team had shown that retinal detachment without oxygen supplementation caused the death of some of the photoreceptors; the loss of cytochrome oxidase from the inner segments and the collapse of the outer segments of surviving photoreceptors; the loss of the synaptophysin profiles from the outer plexiform layer; and the loss of bFGF protein from retinal neurons and neuroglia, but not from retinal vessels. Using the oxygen techniques developed at Sydney, the teams showed that oxygen supplementation during detachment mitigated all these changes, reducing photoreceptor death, maintaining the specialized structures of surviving photoreceptors and stabilizing the bFGF protein within the retina.
“The optimistic inference drawn from this idea is that the clinical management of detached retina may be improved by measures that control the pathology of detachment, specifically by measures that counter the factors activating suicide and deconstruction mechanisms,” researchers wrote. “The present results indicate that hypoxia is such a factor and suggest an intervention like oxygen supplementation between diagnosis and reattachment surgery that may counter it.”
Müller cells
To further assess the role of hypoxia following retinal detachment, the joint teams studied the proliferation, hypertrophy and dysfunction of Müller cells — cells that proliferate sharply within 3 or 4 days of a retinal detachment — was studied in the same material, but using techniques to detect cells which proliferate. This was of interest because the eye can be blinded by proliferative changes, even after successful reattachment surgery. The teams concluded that oxygen supplementation reduced the reaction of the retinal Müller cells to retinal detachment, limiting their proliferation and helping to maintain their normal structure and function.
“In the clinical setting, oxygen supplementation between the diagnosis and reattachment surgery may reduce the incidence and severity of complications such as proliferative vitreoretinopathy,” they wrote.
Both studies appeared in the August 1999 issue of the American Journal of Ophthalmology.
For Your Information:Reference:
- For more information on Dr. Mervin’s or Dr. Lewis’s study, contact Prof. J. Stone, New South Wales Retinal Dystrophy Research Centre, Department of Anatomy and Histology, University of Sydney F1-3, New South Wales 2006, Australia; fax: (61) 2-93-51-56-64; e-mail: jonstone@anatomy.usyd.edu.au.
- Mervin, et al. Limiting photoreceptor death and deconstruction during experimental retinal detachment: the value of oxygen supplementation. Am J Ophthalmol. 1999;128:155-164.
- Lewis, et al. Limiting the proliferation and reactivity of retinal Müller cells during experimental retinal detachment: the value of oxygen supplementation. Am J Ophthalmol. 1999;128:165-172.