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Br J Ophthalmol 2002;86:227-232 doi:10.1136/bjo.86.2.227
  • Original Article
    • Clinical science

Systemic vascular endothelial cell dysfunction in normal pressure glaucoma

  1. Christine Buckley1,
  2. Patrick W F Hadoke2,
  3. Emer Henry3,
  4. Colm O'Brien4
  1. 1Department of Medicine, Royal Infirmary of Edinburgh, UK
  2. 2Department of Medical Sciences, Western General Hospital, Edinburgh, UK
  3. 3Department of Ophthalmology, Royal Infirmary of Edinburgh, UK
  4. 4Institute of Ophthalmology, University College Dublin, Ireland
  1. Correspondence to: Dr C O'Brien, Mater Misericordiae Hospital, Eccles Street, Dublin 7, Ireland; cobrien{at}mater.ie
  • Accepted 30 April 2001

Abstract

Aim: Vascular risk factors, and particularly vasospasm, are thought to play a part in the pathogenesis of normal pressure glaucoma (NPG). This study aimed to determine whether the function of systemic resistance arteries was altered in patients with NPG.

Methods: Contractile and relaxant function was assessed in arteries dissected from gluteal fat biopsies (11 NPG, 12 control) using small vessel myography.

Results: Responses to K+ and noradrenaline were similar in patients and controls and were unaffected by endothelial removal. In contrast, responses to 5-hydroxytryptamine (5-HT; pD2; 7.29 (SD 0.16) v 6.66 (0.19); p=0.03) and endothelin-1 (ET-1; pD2, 9.12 (0.10) v 8.72 (0.13); p=0.03) were enhanced in arteries from patients with NPG. Removal of the endothelium enhanced responses to 5-HT (pD2, 6.66 (0.19) v 7.66 (0.08); p=0.003) and ET-1 (pD2, 8.72 (0.13) v 9.66 (0.39); p=0.02) in control arteries but not in those from patients. ET-1 mediated contraction in control and patient arteries was reduced in the presence of (10−5 M) nifedipine. Endothelium dependent and independent relaxation was not impaired in arteries from patients.

Conclusions: This study has identified dysfunction of the systemic vascular endothelial cell in patients with normal pressure glaucoma. The vascular endothelium modulates contractile responses to 5-HT and ET-1 in human subcutaneous resistance arteries but this effect is lost in patients with NPG, indicating a selective defect in agonist mediated release of endothelium derived vasodilators. Selective antagonists of 5-HT and ET-1 may, therefore, help to prevent vasospasm in patients with NPG.

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