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Systemic vascular endothelial cell dysfunction in normal pressure glaucoma.

Christine Buckley1, Patrick W F Hadoke, Emer Henry

  • 1Department of Medicine, Royal Infirmary of Edinburgh, UK.

The British Journal of Ophthalmology
|January 30, 2002
PubMed
Summary
This summary is machine-generated.

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Patients with normal pressure glaucoma (NPG) exhibit impaired systemic vascular endothelial function. This dysfunction affects responses to specific agonists, suggesting a potential target for preventing vasospasm in NPG.

Area of Science:

  • Ophthalmology
  • Vascular Biology
  • Glaucoma Research

Background:

  • Vascular risk factors, including vasospasm, are implicated in normal pressure glaucoma (NPG) pathogenesis.
  • Systemic resistance artery function in NPG patients requires further investigation.

Purpose of the Study:

  • To investigate alterations in systemic resistance artery function in patients with normal pressure glaucoma.
  • To determine if vascular endothelial function is compromised in NPG.

Main Methods:

  • Small vessel myography was used to assess contractile and relaxant function.
  • Arteries were obtained from gluteal fat biopsies of 11 NPG patients and 12 controls.
  • Responses to potassium chloride, noradrenaline, 5-hydroxytryptamine (5-HT), and endothelin-1 (ET-1) were analyzed.

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Main Results:

  • Arteries from NPG patients showed enhanced responses to 5-HT and ET-1 compared to controls.
  • Endothelial removal augmented 5-HT and ET-1 responses in control arteries, but not in NPG arteries.
  • Endothelium-dependent and independent relaxations were not impaired in NPG patients' arteries.

Conclusions:

  • Systemic vascular endothelial cell dysfunction is identified in patients with normal pressure glaucoma.
  • The endothelium's modulatory effect on contractile responses to 5-HT and ET-1 is lost in NPG patients.
  • This suggests a defect in agonist-mediated release of endothelium-derived vasodilators, potentially treatable with selective 5-HT and ET-1 antagonists.