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(Investigative Ophthalmology and Visual Science. 1999;40:1710-1714.)
© 1999 by The Association for Research in Vision and Ophthalmology, Inc.

Peripheral Endothelial Dysfunction in Normal Pressure Glaucoma

Emer Henry1,2, David E. Newby2, David J. Webb2 and Colm O’Brien1

1 From the Princess Alexandra Eye Pavilion, Edinburgh; and the 2 Clinical Pharmacology Unit, Western General Hospital, Edinburgh.

PURPOSE. To assess vascular endothelial function in patients with normal pressure glaucoma using forearm blood flow responses to intra-arterial infusions of endothelial-dependent and -independent vasoactive agents.

METHODS. Eight patients with newly diagnosed and untreated normal pressure glaucoma and eight healthy age- and sex-matched control volunteers underwent measurement of forearm blood flow using venous occlusion plethysmography. Blood flow was assessed in response to incremental doses of sodium nitroprusside (an endothelial-independent vasodilator), acetylcholine (an endothelial-dependent vasodilator) and the vasoconstrictor NG-monomethyl-L-arginine (an inhibitor of nitric oxide synthase).

RESULTS. Sodium nitroprusside caused a dose-related increase in forearm blood flow in patients and controls. Glaucoma patients appeared to have an increased vasodilatory response, but this was not significant (P = 0.23). Acetylcholine also induced vasodilatation in both groups, but the response was significantly reduced in the glaucoma group (P = 0.04). NG-monomethyl-L-arginine induced a similar degree of vasoconstriction in both groups (P = 0.76).

CONCLUSIONS. This study has shown an impairment of peripheral endothelium-mediated vasodilatation in normal pressure glaucoma. These findings would support the concept of a generalized vascular endothelial dysfunction in patients with this condition.




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