St. Louis, Aug. 17, 1999 -- Investigators at Washington University School of Medicine in St. Louis believe they have identified the basis for a new way to treat glaucoma, the second-leading cause of irreversible vision loss in the United States.
In the Aug. 17 issue of Proceedings of the National Academy of Sciences, the investigators report on experiments involving an animal model of glaucoma. Working in rats with elevated eye pressure, they were able to prevent loss of retinal ganglion cells by inhibiting the action of an enzyme that makes nitric oxide.
"Having seen reports on nerve damage caused by excessive nitric oxide, we decided to look for evidence of high levels of nitric oxide in human eyes with glaucoma," said lead author Arthur H. Neufeld, Ph.D., the Bernard Becker Research Professor of Ophthalmology and Visual Sciences. "Using sophisticated staining techniques, we detected an enzyme called inducible nitric oxide synthase in the optic nerve head tissue of patients with glaucoma."
This enzyme -- NOS-2 -- can produce excessive amounts of nitric oxide, and Neufeld and colleagues regarded its presence as evidence that nitric oxide might be involved with the ganglion cell damage seen in glaucoma. To explore that idea, they set out to determine whether NOS-2 was causing the damage in retinal cells or appearing as a byproduct of that damage.
"We adopted an animal model of glaucoma that raises pressure levels in the eyes of rats," Neufeld said. "And we found that, as in humans, the eyes of rats with elevated pressure lost retinal ganglion cells and that the tissue also contained elevated levels of NOS-2."
For the last century, most medical and surgical therapies for glaucoma have
attempted to lower pressure in the eye, aiming to prevent or delay damage to
ganglion cells and preserve good vision. "But we have many clinical situations
where we can't get the pressure low enough to avoid damage," said Bernard
Becker, M.D., professor
Contact: Jim Dryden
Washington University School of Medicine