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Published on: March 12, 2016
Altered nitric oxide system in patients with open-angle glaucoma.
Kaija Polak1, Alexandra Luksch, Fatmire Berisha
1Department of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria.
Archives of Ophthalmology (Chicago, Ill. : 1960)
|April 11, 2007
Summary
Patients with primary open-angle glaucoma show an altered ocular blood flow response to nitric oxide synthase inhibition. This suggests potential benefits from normalizing nitric oxide production for ocular blood flow and neuroprotection.
Area of Science:
- Ophthalmology
- Cardiovascular Research
- Neuroscience
Background:
- Primary open-angle glaucoma (POAG) is a leading cause of irreversible blindness.
- Ocular blood flow dysregulation is implicated in POAG pathogenesis.
- The role of the L-arginine/nitric oxide (NO) pathway in ocular hemodynamics of glaucoma is not fully understood.
Purpose of the Study:
- To investigate the ocular blood flow response to systemic nitric oxide synthase (NOS) inhibition in POAG patients.
- To compare these responses with age-matched healthy controls.
Main Methods:
- 12 POAG patients and 12 controls underwent measurements of subfoveal choroidal blood flow, optic nerve head blood flow, ocular fundus pulsation amplitude, intraocular pressure, and systemic hemodynamics.
- NOS was inhibited via intravenous administration of NG-monomethyl-L-arginine (L-NMMA).
Main Results:
- Systemic blood pressure response to L-NMMA was similar between groups.
- Glaucoma patients exhibited significantly less pronounced decreases in optic nerve head blood flow (P=.03) and fundus pulsation amplitude (P<.001) during NOS inhibition compared to controls.
- A trend towards a reduced choroidal blood flow response was observed in glaucoma patients (P=.051).
Conclusions:
- This study provides the first in vivo evidence of an altered ocular L-arginine/NO system in POAG.
- Modulating ocular NO production may normalize ocular blood flow and offer neuroprotection to retinal ganglion cells in glaucoma.
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