Pharmacologic neuroprotection with an inhibitor of nitric oxide synthase for the treatment of glaucoma.
Excessive nitric oxide, generated by inducible NOS-2 in astrocytes and microglia in the optic nerve head of patients with glaucoma, may contribute to the optic neuropathy associated with the disease. A rat model of glaucoma, in which there is chronic, moderately elevated IOP and slow loss of retinal ganglion cells, has been established to study pharmacological agents that have the potential to be neuroprotective. In this model, the pharmacological use of an inhibitor of NOS-2, aminoguanidine, significantly prevents the loss of retinal ganglion cells. A well-tolerated pharmacological inhibitor of NOS-2, perhaps orally or locally delivered, is a reasonable candidate for a neuroprotective agent for treating glaucoma.
Neufeld
Arthur H
AH
Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, 660 South Euclid Avenue, Box 8096, St. Louis, MO 63110, USA. neufeld@vision.wustl.edu
D000818:Animals; D004791:Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D005901:Glaucoma / Q000188:drug therapy* / Q000201:enzymology; D006801:Humans; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors* / Q000378:metabolism
D004791:Enzyme Inhibitors; D018696:Neuroprotective Agents; D019001:Nitric Oxide Synthase