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PURPOSE: Vasospasm, resulting from a generalized dysfunction in the vascular endothelium, is implicated in the development of normal-pressure glaucoma (NPG). Impaired endothelium-derived nitric oxide activity and abnormalities of the endothelin system suggest systemic endothelial cell dysfunction in patients with NPG. Endothelin (ET)-1 vasoreactivity was assessed in the peripheral circulation of patients with NPG. METHODS: Forearm blood flow was measured using venous occlusion plethysmography in eight patients with untreated NPG and eight age- and sex-matched healthy volunteers during intra-arterial infusion of ET-1 (5 pmol/min) and, on a separate occasion, to BQ123, a selective endothelin-A receptor antagonist, (100 nmol/min). Blood pressure and heart rate were measured in the noninfused arm, and plasma ET-1 concentrations were measured using a radioimmunoassay. RESULTS: Forearm blood flow fell during infusion of ET-1 (P < 0.001 for both) to a similar extent in both groups (P = 0.7; patients versus control subjects). In contrast, BQ123 increased forearm blood flow in both groups (P < 0.001 for both), although the vasodilatation was lower in patients than in control subjects (P < 0.001; patients versus control subjects). There was no difference in basal plasma ET-1 concentrations between the two groups (P = 0.81; patients versus control subjects). CONCLUSIONS: Despite normal responses to ET-1, patients with NPG have reduced vasodilatation in response to ET(A)-receptor antagonism. This could be due to attenuated ET(A)-receptor-mediated tone, increased ET(B)-receptor-mediated contraction or impaired ET(B)-receptor-mediated release of endothelial nitric oxide. These results are consistent with the authors' previous demonstration of systemic vascular dysfunction in patients with NPG.
Dr. E. Henry, Princess Alexandra Eye Pavilion, Edinburgh, UK
6.11 Bloodflow measurements (Part of: 6 Clinical examination methods)
9.2.4 Normal pressure glaucoma (Part of: 9 Clinical forms of glaucomas > 9.2 Primary open angle glaucomas)